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7.1 CONCEPTS
7.1.1 Epidemiological Characterization
7.1.2 The Agent: Micro-Organism
7.1.3 The Host
7.1.4 The Disease
7.1.5 Control and Prevention of Communicable Disease
7.2 VIRUSES
7.2.1 Viral Infections: Feco-Oral
7.2.2 Viral Infections: Air-Borne
7.2.3 Viral Infections: Vector-Borne
72.4 Viral Infections: Parenteral
7.2.5 Viral Infections: Others
7.3 PROKARYOTES
7.3.1 Bacteria Infections: Feco-Oral
7.3.2 Bacterial Infections: Droplet Spread
7.3.3 Bacterial Infections: Sexually Transmitted
7.3.4 Bacterial Infections: Others
7.3.5 Chlamydial & Rickettsial Infections
7.4 EUKARYOTES
7.4.1 Protozoal Infections
7.4.2 Helminthic Infestations
7.4.3 Fungal Infections
7.5 EMERGING and RE-EMERGING INFECTIONS
7.5.1 Over-View
7.5.2 Sexually Transmitted Diseases
7.5.3 Viral Diseases
7.5.4 Bacterial Diseases
7.5.5 Parasitic Diseases:
UNIT 7.1
CONCEPTS
Learning Objectives:
· Incidence and prevalence
· Attack rates (primary & secondary), case fatality ratio.
· The causal triangle: agent (types of micro-organisms, transmission routes with examples for each route), host (susceptibility), and disease (natural history, clinical features)
· Methods of transmission
· Difference between control and eradication of communicable disease
· Prevention of communicable disease (primary, secondary, tertiary) and surveillance
· Investigation and management of a disease out-break
7.1.1 EPIDEMIOLOGICAL CHARACTERIZATION
A. Definitions
B. Communicable Disease Model
C. Rates & Proportions
D. Epidemiology
E. Trends of Incidence
7.1.2 THE AGENT: MICRO-ORGANISM
A. Complex Interactions
B. Classification of Microorganisms
C. Description of Major Groups of Microorganisms
D. Transmission
E. Environment-Related Factors
7.1.3 THE HOST
A. Humans Hosts:
B. Susceptibility:
C. Spread of Infection
D. Host Response
7.1.4 THE DISEASE
A. Clinical Severity
B. Clinical Manifestations
C. Natural History
D. Epidemicity
E. Epidemiological Models
7.1.5 CONTROL and PREVENTION OF COMMUNICABLE DISEASE
A. Control Strategy
B. Primary Prevention
C. Secondary Prevention
D. Tertiary Prevention
E. Control of Disease Outbreak
F. Breaking the Transmission Cycle by Type of Disease
7.1.1 EPIDEMIOLOGICAL CHARACTERIZATION
A. DEFINITIONS
Infectious disease is disease transferred from person to person by micro-organisms. Infectious disease results from the action of the infectious agent or its products. The terms communicable disease and infectious disease are synonymous. Infection is the process of lodging, growing, and multiplication of micro-organism in host’s body. Invasion is mere presence of micro-organism in body of host without necessarily multiplying. Infestation is . Infectivity is the ability of the infective agent to lodge and grow in the host. Pathogenicity is the ability of the organism to cause disease and is measured as the proportion of the number of infected poersons with clinical disease to the total number of infected person. Virulence is the ability to cause severe disease. The measles and varicella zoster viruses are very pathogenic but not virulent. HIV is very virulent since all those affected eventually die. Pathogenicity is affected by invasiveness, toxigenicity, and hypersensitivity. Some organisms like shigella invade tissues. Others like Cl. Botulinum produce toxins. Mycobacterium tuberculosis causes hypersensitivity or allergic reactions in the host. An epidemic is said to occur when the epidemic threshold is breached. The term epidemic is used to refer to a wide-spread disease whereas the term outbreak is used to refer to localized disease.
B. COMMUNICABLE DISEASE MODEL
THE TRIAD
The communicable disease model comprises of the three minimum factors needed for occurrence and spread of disease: the agent, the host, and the environment. The environment, physical or biological, may inhibit or promote disease transmission. Disease transmission occurs when a susceptible host and a pathogenic agent exist in an environment conducive to disease transmission.
GASTRIC INFECTION – PEPTIC ULCER
Peptic ulceration is a problem in both developed and less developed countries. The disease is a result of interplay of genetic and environmental factors. Death from PU complications rises with age. H. pylori infection and use of non-steroidal anti-inflammatory drugs are factors determining severity of the disease. Smoking increases the risk of PU. There is no evidence for the role of diet or stress in PU. H. pylori infection is found in association with PU. Its eradication leads to subsiding of PU symptoms. PU infection is acquired in childhood due to poor sanitation. Most of those infected do not develop the ulcer. The risk of H.pylori infection is falling in Europe and America
INTESTINAL INFECTION
Intestinal infections present as watery diarrhoea, bloody diarhoea (dysentery), or chronic diarrhoea with or without steatorrhoea. Watery diarrhoea is self limiting and resolves within 5-7 days. It requires only fluid and electrolyte replacement. Dysentery and chronic diarrhoea require specific treatment. The prevalence of intestinal infections is higher in less developed countries because of poor sanitation, water shortage, poor hygiene, and crowding. Intestinal infections still accounts for substantial morbidity in developed countries. Intestinal infection in the US
The following are factors in intestinal infection: travel, immunodeficiency, institutional living, dat care, reduced gastric acid secretion, extremes of age, swimming, eating raw fish, eating partially cooked eggs, and eating myonnaise. Intestinal infections are transmitted by the feco-oral route. Humans are the major reservoirs of intestinal infections. Salmonella spp and Cl. Jejuni are exceptions because they have animal reservoirs. The majority of bacterial enteropathogens have seasonality. Cholera occurs more in the rainy season. Parasites occur more in winter because their cysts can survive better in the cold climate. Ritavirus infection is more common in the winter. Intestinal infections are prevented by interrupting the fecal-oral transmission route. Thus is achieved by using clean potable water, safe fecal disposal, personal hygiene, and food hygiene. Propyhllatic antibiotics can be used at half the therapeutic dose. Vaccination can be carried out for cholera, salmonella spp. and shigella spp. The evidence for probiotics in prevention is not definitive.
C. RATES & PROPORTIONS
The primary attack rate is defined as the number of new cases of disease expressed as a proportion of the total susceptible population. The secondary attack rate is defined as the number of additional cases of disease among contacts of the primary or index cases within the maximum incubation period expressed as proportion of the total number of susceptible contacts. The case fatality ratio is number of fatal outcomes expressed as a proportion of the total number of cases with symptomatic illness.
D. EPIDEMIOLOGY
Correct and complete incidence and prevalence on communicable diseases is not available for many diseases. This is due to incomplete reporting and non-detection of sub-clinical cases.
E. TRENDS OF INCIDENCE
Most morbidity & mortality in the world is due to microbials. Most of this mortality and morbidity is in the less developed countries of Asia, Africa, and Latin America . Infection patterns differ according to level of economic development. Less developed countries have higher incidence and prevalence of infectious diseases than the developed countries. Most less developed countries are experiencing a falling incidence of infection and mortality due to socio-economic improvement, specific and non-specific primary prevention (sanitation and immunisation). In both LDC and industrialised countries, old diseases like small poxes are being controlled. Some old ones like TB and syphilis are re-emerging. New diseases related to lifestyle like HIV and other STDs are appearing and are increasing.
7.1.2 THE AGENT: MICRO-ORGANISM
A. COMPLEX INTERACTIONS
The interaction between human tissues and microorganisms is very complex. The most successful parasites do not destroy their human hosts. The profile of disease-causing microorganisms is changing. New agents are being discovered. Some old agents are being eradicated. New pathogenic effects are being discovered for old known agents. Some agents are undergoing changes in pathogenicity. Organisms like the influenza virus can avoid host immune defences because of their frequent antigenic shift. Many microorganisms like N. gonorrhea have developed resistance to antibiotics.
B. CLASSIFICATION OF MICROORGANISMS
There are several approaches to classification of microorganisms: cellular complexity, method of transmission, ability to cause disease, and method of interaction with humans. According to cellular complexity microorganisms can be classified as pro-karyotes, eucaryotes, and viruses. Prokaryotes comprise bacteria, rickettsiae, and chlamydia. Eucaryotes comprise fungi, protozoa, and helminths. Viruses are chemical entities with only rudimentary functions of life. Microorganisms can be classified according to the method of transmission. There are several methods of transmission: feco-oral, soil contact, water contact, skin contact, air transmission, contact with body fluids, and arthropod-borne transmission. Examples of organisms transmitted by the feco-oral metjhods are ameba, giardia, shigella, vibrio cholera, salmonella spp, hepatitis virus A&E, polio virus, and tapeworms. Examples of microorganisms transmitted by the soil are trichuris, ascaris, hookworms, strongyloides, and tetanus. Examples of microorganisms transmitted by water contact are schistosomiasis and guinea worm. Examples of microorganisms transmitted by contact with infectious skin rashes are chickenpox and smallpox. Examples of organisms transmitted by inhalation are measles, pertussis, diphtheria, and tuberculosis. The following microorganisms are transmitted by contact with infected body fluids: trachoma, syphilis, gonorrhoea, and HIV. Arthropod vectors transmit the dengue virus and the malarial protozoan. Microorganisms can be classified according to their ability to cause disease. The following parameters are used: infectivity, virulence, pathogenicity, toxigenicity, and the infective dose. Microorganisms can be classified according to their mode of interaction with the human host as saprophytic, parasitic, and symbiotic. Saprophytes live on dead organic matter. Parasites are dependent on the human host either as harmless commensals or as pathogenic parasites. Obligate parasites cannot exist outside their host. Non-obligate parasites are able to pursue an independent existence of they cannot find a host. Symbiotic relations involve mutualism and are mutually beneficial. Normal flora is bacteria in the body described as opportunist pathiogens. They are found in the mouth, URT, GIT, urethra, vagina, and the conjuctiva. They are beneficial to the body by preventing colonisation by pathogens as well as vitamin K synthesis. Normal flora can become opportunistic infections when they are in unusual sites or in conditions of reduced immunity.
C. DESCRIPTION OF MAJOR GROUPS OF MICROORGANISMS
VIRUSES
Viruses are obligate intracellular parasites. They take over and use the cell's metabolism for their own replication. They are most vulnerable during transmission to and from the host. Viral infections are recognized by detection of viral antigens or antibodies to viral antigens. Among the commonly used serological techniques are: neutralization, hemagglutination inhibition, complement fixation, fluorescent antibody, radioimmunoassay, and ELISA. Small amounts of viruses can also be detected by cell culture.
BACTERIA
Normal healthy individuals have a lot of bacteria most of which are harmless normal flora that prevents colonization by pathogenic bacteria. Bacteria may produce pathogenicity by direct action on the tissues, producing toxins, proteases, and cytolysins. Bacteria adhere to specific sites on the cell and initiate damage of the cell wall and gain entrance to the interior of the cell. Enterotoxins act on intestinal villi to cause diarrhoea. Toxins produced by vibrio cholerae, clostridium, tetanus, diphtheria, and anthrax bacteria have various effects on body tissues. Bacteria can be destroyed in the blood stream before entering cells by humoral or cell-mediated immune defence mechanisms. Adherence to the cell wall may be blocked by antibodires. Bacteria have developed methods of avoiding desrruction both outside and inside the cell. Encapsulation provides protection against physical elements. Antibiotic resistance mediated by plasmids and other mechanisms protects against antibiotic effects. Diagnosis of bacterial infections is based on cultivation & identification, gram staining & microscopy, biochemical reactions, use of specific antibodies, and DNA hybridization.
FUNGI
Fungal infections are comparatively less common than viral, bacterial, protozoal, or helminthic infections. Fungal infection is usually by direct contact with the soil or inhalation from the air. Person to person transmission of fungal infections is rare, the exception being dermatophytoses. The route of transmission determines the form of disease. Cutaneous and muco-cutaneous infection follows direct contact with the soil. Pulmonary disease is due to air inhalation. Fungal infections are usually localized. Systemic infections are rare but could occur and in a severe form in cases of malignancy and other causes of immune deficiency. Fungi can cause disease on ingestion in food. Examples of fungal poisons, mycotoxins, are amanita phalloides, a type of mushroom, aflatoxins and aspergillus flavus. Diagnosis of fungal infection is difficult and is based on clinical or histological examination.
PROTOZOA
Protozoa are single-celled eucaryotic organisms widely distributed in the world in both parasitic and free-living forms. Protozoa have developed ways of avoiding host immune defences but are prudent enough not to destroy the host on whom they depend. This explains the high prevalence of protozoal infections but low morbidity levels. The following are protozoal species that are epidemiologically most important: plasmodium, toxoplasma, and pneumocytes. Plasmodia cause malaria that is the most important protozoal disease in terms of mortality and morbidity. P. falciparum causes more mortality and morbidity and is more important epidemiologically than the 3 other plasmodial species: P.ovale, P. vivax, and P. malariae. Red blood cells with HB-S, HB-F, or G6PD deficiency have natural resistance to malarial infection. T.gondi is another protozoal infection with a high prevalence with little clinical disease. P. carinii is wide-spread and has become important epidemiologically because it is an opportunistic infection complicating HIV/AIDS.
HELMINTHS
There are 3 types of helminths: flat worms also caled cestodes, flukes also called trematodes, and roundworms also called nematodes. Helminths are widely distributed in the world but most species are in the tropics. Helminths can reside in human hosts for years producing eggs or larvae. They however cannot complete their life cycle in the human host. They have to live in the soil or other hosts for part of the lifecycle. Helminths are transmitted by vertebrate or invertebrate vectors. Helminths that migrate in the blood stream or that invade tissues can elicit an immune response. Those that infest the intestines elicit no immune response. The most important helminths from the epidemiological perspective are: schistosomiasis, hookworm, stringyloides, echinococcus, tenia, and toxicara. Schistosomiasis is of major worldwide epidemiological importance. Hookworm by causing chronic blood loss is responsible for a lot of malnutrition. S.stercoralis can live freely but also as a human parasite being able to live asymptomatically in the human body for 30 years or more. Strongyloides commonly causes intestinal disease; pulomnary disease occurs but is rare. It is associated with severe morbidity and mortality in immune-compromised persons. The larval stages of the following helminths are of epidemiological importance: echinococcus granulosus causing hydatid disease, echinococcus multiocularis causing hydatid disease, tenia solium causing cysticercosis, and toxacara canis causing visceral larva migrans.
D. TRANSMISSION
SURVIVAL
During part of its lifecycle, the microorganism passes from one human host to another. It can also pass from the outside environment to the human host and vice versa. In a group of diseases called zoonoses, transmission is from animal to the human host. It is most vulnerable to destruction during the stage of transmission to the host. Microorganisms can survive adverse conditions and be transmitted by living in reservoirs, persistence in spores, latency, and growing in the vector or an intermediate host. Resrvoirs can be humans, animals, or the soil.. Clostridia are bacteria that can survive long periods in the soil in an encapsulated form. EBV and CMV are examples of microorganisms that survive for a long time in a latent form.
RESERVOIRS
Some microorganisms survive in reservoirs until they can infect humans. These reservoirs are intermediate animal hosts required to complete the lifecycle. Reservoirs that do not get diseased are more dangerous for humans because eradication is more difficult. Diseases without reservoirs are easier to eradicate. This explains the eradication of small pox because it has no natural resrvoir. There are about 150 zoonoses. Direct zoonoses require only one animal reservoir for example rabies, brucellosis, and trichnosis. Cyclozoonozes like the tapeworm require at least 2 vertebrate species to complete the life cycle. Metazoonoses like the schistosoma helminth and the yellow fever virus require an intermediate invertebrate host. Saprozoonoses like coccidiomycosis require an inanimate intermediary in addition to an animal reservoir.
VECTORS
Vectors are organisms that tranfer the microorganisms. The transmission may be mechanical (eg flies and cockroaches) or hematophangous (eg ticks, lice, fleas, mites). Hematophagous transmission involves growth and replication in the vector. Replication within the host increases the number of infective microorganisms and thus enhances the infection potential.
ROUTES OF TRANSMISSION, SOURCES OF INFECTION and PORTALS OF ENTRY and EXIT
Transmission is described as common vehicle spread for example by water, air of food or as serial transmission when it is human to human, human to animal to human, or human to the environment to human. Transmission may be direct or indirect. Indirect transmission may be vehicle-borne eg by fomites, vector-borne (mechanical and biological) or airborne (droplets or dust). Infection can be exogenous or endogenous. Exogenous infection is from outside the body of the host. It can be from humans, transient or chronic carriers, or the environment. Endogenous infection is from within the body of the host. The phenomenon of auto-infection found in strongyloides and E.coli are examples of auto-infection. Disease transmission may be horizontal or vertical; the horizontal being more common. Horizontal transmission is from one human to another. Vertical transmission is intra-uterine from the mother to the fetus. The natural portals of entry into human are the respiratory tract (common cold, influenza, measles, TB, whooping cough), the urogenital tract (gonorrhoea, syphilis, herpes, HIV), the alimentary tract (amebic dysentery, shigellosis, polio, and cholera), the mucous membranes, the skin, the placenta (rubella, syphilis, and HBV), and the parenteral portal (intravenious and sexual). The skin is a good natural barrier to infection but can be penetrated by insects, ticks, needles, and traumatic injuries. The chain of infection starts with the pathogen in the reservoir (case, carrier, animal). It goes out from a portal of exit and is transmitted to the portal of entry. It enters the new host where it is established to cause disease.
HORIZONTAL TRANSMISSION
Horizontal transmission may be direct or incirect. Direct horizontal transmission causes immediate infection and occur in 4 forms: direct contact with the skin by biting or touch (eg hookworm), inoculation of the micro-organism (eg STD), ingestion of the micro-organism in food, drink, or contact with fomites (eg E.coli), and aerial/droplet spread (eg measles). Indirect horizonal transmission may be airborne, vehicle-borne, or vector-borne. The involvement of an intermediate host or vector causes delayed disease. Air-borne infections are carried as microbial erosols for example TB, influenza, histoplasmosis, and legionellosis. Vehicle borne transmission is by contaminated materials or objects (fomites) for example toys, handkerchiefs, soiled clothes, beddings, food service utensils, surgical instruments, water, blood, milk, organs and tissues. The vectors may be arthropods (such as mosquitoes, fleas, flies, lice, and ticks), zoonoses, plants, or other vehicles. They transmit organisms either mechanically or biologically. Dysentary and polio are examples of mechanical transmission. Biological transmission is more common than mechanical transmission. Arthropods transmit microorganisms from one animal to another with humans being only accidental hosts like in plague. Mosquitoes transmit yellow fever, dengue, and malaria. Flies transmit African trypanosomiasis, onchocerciasis, loaiasis, and leishmaniasis. Ticks transmit rock mountain spotted fever, relapsing fever, and Lyme disease. Fleas transmit plague, and murine tyohus. Lice transmit epidemic typhus and trench fever. Kissing bugs transmit Chagga’s disesse. Zoonoses are diseases of whose reservoirs are vertebrates animals and are transmitted to humans by accident for example plague, rabies, rocky mountain spotted fever. Antrhoponooses are diseases whose reservoirs are human for example measles. Plants can be vectors of disease when they are contaminated by micro-organisms and are eaten raw.
VERTICAL TRANSMISSION
The vertical route of disease transmission is trans-placental transmission in utero. It is thought but not yet decisively proved that the following organisms can be transmitted vertically: ?CMV, ?toxoplasma, ?rubella, ?HSV, ?syphilis, ?TB, ?VZ.
MATHEMATICAL MODELS OF DISEASE TRANSMISSION
We can predict microbial transmission using mathematica models that have been developed from empirical observations. The factors of transmission probability are: the infected host, the susceptible host, contact, and the parasite. The basic reproductive number, R0, is the number of contacts per unit time x transmission probability per unit time x duration of infectiousness. An approximate formula for the basic reproductive number is R0 = 1 + L/A where L = average lifespan of an individual in the population and A = average age at infection. The serial interval or generation time is the time between two generations of infection.
E. ENVIRONMENT-RELATED FACTORS
The concept of the communicable disease triangle simplifies discussion of communicable disease. The triangle consists of the agent, the host, and the disease. They interact among one another. Elements of the environment that affect disease transmission are: climate (temperature, rain, wind patterns), vegetation (swamps, forest, and desert), water sanitation, air pollution, excreta disposal, housing, occupation (farm, factory). Poor sanitation and crowding increase the transmission of microorganisms. Breeding places near homes, forest reservoirs, and soil help the survival of organisms and their vectors.
7.1.3 THE HOST
A. HUMANS HOSTS:
Humans can be hosts of microbial infection in the following forms: intermediate host, definitive host, ?reservoir host, and accidental host. Humans can also be in a carrier status. They can be healthy, incubational, convalescing, or chronic carriers. Healthy carriers remain free of the disease while transmitting it to others; for example polio is transmitted by healthy carriers. HIV and HBV can be transmitted by incubationary carriers who are infectious before symptoms and signs of disease appear in them. Typhoid is transmitted by convalescing carriers. The human host has mechanisms to prevent the establishment of infection. These include: seborrhoeic acid in the skin and vaginal glycogen that is metabolized by lactobacilli to produce lactic acid.
B. SUSCEPTIBILITY:
Susceptibility to infection is determined by age, heredity, gender, pregnancy, nutritional status, life-style and behavior, personal hygiene, and immune resistance. Age determines disease risk at the extremes of life. The very young and the elderly are immuno-incompetent and are more likely to be infected and also to experience more severe disease. Polio, hepatitis A, and infleunza are an exception to this general rule being less severe in the young. Influenza is definitely more severe in the elderly. Heredity determines immune resistance. Gender differences have been observed for many diseases. The susceptibility and attack rates for some diseases also vary by gender. The variation may be due to behavior or may be biological. Females enjoy an immunological superiority that may partially explain their longevity. Some diseases like RSV are more severe in boys. Pregnancy is a state of immuno-incompetence that favours infection. Childbirth is a period of increased susceptibility to genital tract infection. The nutritional status affects immune competence. Under-nutrition in the form of protein energy malnutrition, PEM, or micro-nutrient deficiencies causes immune incompetence. Life-style and behaviour affect exposure to infectious agents. The type of food eaten and pets kept may determine what micro-organisms a person is exposed to. Personal hygiene is important in ridding the body of likely pathogenic organisms. Immune resistance is the main barrier to infection by micro-organisms. Immunity may be natural (innate) or acquired. Natural immunity is non-specific and is based on cellular barriers (NK cells and phagocytes such as macrophages, polymorphs, and reticuloendothelial cells), mechanical surface barriers (skin, mucous membranes, cilia, the cough angf gag reflexes), physiological barriers (fever), chemical barriers (stomach acidity, acidity of vagina, hydrolytic and proteolytic enzymes in the saliva and intestines, and biologically active substances like enzymes, lipids, & interferon), and inflammation. Acquired immunity to disease, cell mediated or humoral, develops as children grow into adulthood. Immunocytes are either T or B lymphocytes whose progenitors are in the bone marrow. Acquired immunity may be active or passive. Passive acquired immunity is based on maternal antibodies or therapeutic intervention by use of immune serum, cytokinase, or anti-toxins. Passive immunity occurs when formed antibodies are given either transplacentally or by post-natal vaccination. Some infections do not occur in the first 6 months of life because of passive immunity due to maternal antibodies secreted into milk and colostrum. Immunization against such diseases is not effective before the age of 6 months. Adoptive immunization is still in the experimental stage; it involves transfer of immunocytes from one person to another. Active acquired immunity occurs when antigens are given to stimulate antibody production. The vaccine may be in the form of killed micro organism or its products, modified microorganism, or toxoid. Primary immune deficiency is due to hereditary disorders. Acquired immune deficiency is due to infection, cancer, drugs, malnutrition, and pregnancy.
C. SPREAD OF INFECTION
Spread of infection (number of new cases) is determined by the number of infected persons in the population and the degree of contact between the infected and the susceptibles. The number of susceptibles in the population is increased by birth and in-migration. It is decreased by death of cases, increased immunity, and out-migration.
D. HOST RESPONSE
Fever is a non-specific immune defence mechanism that slows down the multiplication of the agent. Interferon blocks the intracellular multiplication of viruses.
7.1.4 THE DISEASE
A. CLINICAL SEVERITY
Clinical severity can be described as mild, moderate, severe, and fatal.
B. CLINICAL MANIFESTATIONS
Clinical manifestations are: asymptomatic, latent, sub-clinical, and clinical.
C. NATURAL HISTORY
Natural history describes the evolution of the disease process starting from initial infection until cure or development of chronic sequelae. Four stages are described in natural history: the pre-pathogenesis stage is operation of the risk factors, the pre-clinical stage is when disease is initiated but there are no symptoms or signs. The clinical stage is when symptoms and signs manifest. The chronic stage is when complications and permanent deformities occur. Three time periods are described in the natural history of disease: the incubation, latent, and communicability perods. The incubation period is from onset of infection to appearance of clinical symptoms. The latent period is from initial infection to infectiousness. The communicability period (infectious period) is the duration when the infected person is infectious.
Two time lines can be drawn to compare the simultaneous evolution of infectiousness and disease.
Infectiousness | Latent Period | Infectious Period | Non-infectious Period | ||
Disease | Incubation Period | Symptomatic Period | No disease Period | ||
Infectiousness and disease are both shown starting at the same point in time, the point of infection. The latent period ends when the person becomes infectious (is can transmit disease to others). Persons in the early symptomatic period are not yet infectious. Some people with no clinical disease may still be infectious. The non-infectious period is reached when the victims are cured, dead, or removed from the population. The no disease period is reached when the victims are dead, removed from the population, become immune or carriers.
D. EPIDEMICITY
Conditions for a communicable disease epidemic: Three conditions are necessary for an epidemic to occur: the pathogenic agent, host susceptibility, and effective transmission. The agent may be new or may be increased in number resulting in an epidemic. Sometimes epidemics occur because of change in the virulence of the agent. An adequate number of susceptible people in the population must exist to sustain and propagate the epidemic. The proportion of the susceptible necessary for epidemic transmission varies with the communicability of the agent. Highly infectious organisms with high communicability will cause epidemics even if the proportion of the susceptible is high. An epidemic cannot occur unless there is an effective means of transmission between the source of the pathogen and the susceptible person (page 269 Jennifer L Kelsey et al Methods in Observational Epidemiology. OUP New York and Oxford
Types of epidemics of infectious disease: the pattern of disease can be described as epidemic, a temporary excessive incidence rate; a pandemic, a worldwide epidemic, or endemic, disease persistently present in a community. Common source epidemics can be point source (1 person) & extended source (2 persons or more). Propagated source are when several foci are established from the primary focus. The Stages of the epidemic are shown on the epidemic time curves: ascending phase, plateau, and descending curve. The epidemic stops when there are no more susceptibles in the population to be infected. An epidemic may be single or may be secular or seasonal. A single epidemic may be single source epidemic or a propagated source epidemic with secondary and tertiary cases. The index case among the primary cases is of special epidemiological importance if identifiable. Arbovirus infection exhibits seasonality that matches mosquito breeding seasons.
E. EPIDEMIOLOGICAL MODELS
In 1760 Daniel Bernouilli was the first to use a mathematical model when he evaluated the effectiveness of variolation. In 1840 William Farr fitted a normal curve on quarterly smallpox data in England and Wales
7.1.5 CONTROL and PREVENTION OF COMMUNICABLE DISEASE
A. CONTROL AND PREVENTION STRATEGIES
CONTROL STRATEGY
The General control strategy consists of: Identification of cause, notification, treatment of cases using drugs, prevention, and surveillance. The differences between control and eradication are shown in the illustration. Only one infectious disease, smallpox, has been eradicated. Efforts are being undertaken to eradicate polio and dracunculosis. In the past several countries attempted tuberculosis and malarial eradication, some succeeded whereas others did not. Those that did not succeed did not have the resources needed for total eradication and they settled for strategies that would control and contain the disease without necessarily eradicating it completely. The complete eradication of small pox is one of the miracles of medical technology of this century. Three strategic approaches are used in infectious disease control: attacking the infectious agent at its source, interrupting transmission, and reducing the number of the susceptible population.
Control measures applied to the healthy host include active immunization, passive immunization, chemoprophyllaxis, behavioral change (sexual, dietary), physical isolation, and increase of host resistance by better nutrition and health care. If the host is already infected the following control measures are applied: chemotherapy, isolation, quarantine, restriction of activity, and behavioral change. Control measures applied to the vector include chemicals, environmental control, and biological control. Measures applied to animal reservoirs of disease include active immunization, restriction of movement or reduction in number, chemoprophyllaxis and chemotherapy. Measures applied to the environment include water sanitation, provision of safe drinking water, excreta disposal, and food sanitation. Measures applied to the causative agent include cleaniliness, refrigeration, disinfection, and sterilization.
Disease notification plays a central role in disease control. The following are notifiable diseases according to CDC: AIDS, anthrax, botulism, brucellosis, cholera, congenital rubella syndrome, diphtheria, encephalitis, gonorrhoea, H. influenzae, Hansen’s disease, leptospirosis, lyme disease, measles, plague, paralytic polio, psitaccosis, rabies, syphilis, tetanus, trichnosis, tularemia, typhoid, and typhus. States notify CDC using the National Electronic Telecommunication System and CDC publishes the results in Morbidity and Mortality Weekly Report.
PRIMARY PREVENTION
Primary prevention is prevention of initial contact and/or infection. Its objectives are elimination of the source by inactivating the agent, prevention of transmission, and raising the immunological status of the potential host. The agent can be inactivated by physical methods (heat, cold, or radiation) or by chemical methods (chlorination and disinfection). The chain of transmission can be broken by avoiding or destruction of animal and insect vectors and reservoirs including use of insecticides (adulticides, larvicides), repellents, personal protection eg mosquito nets, and biological control; environmantal control of air and dust; personal, domestic, and environmental hygiene; chemoprophyllaxis; detection and treatment of disease; qurantine and isolation; contact tracing; cooking and safe storage of food; safe drinking water; proper excreta disposal; good housing; quarantine and isolation. There are 4 types of disease isolation: strict isolation, contact isolation, respiratory isolation,and enteric isolation. Strict isolation requires a room with special ventilation and is used for pharyngeal diphtheria, viral hemorrhagic fevers, pneumonic plague, smallpox, varicella, and zoster. Contact isolation requires a special room with use of a face mask and is used for major wound or burn infections and acute upper respiratory infections. Enteric isolation requires special handling of waste and articles. .Host immune resistance can be increased by use of specific immunobiologics (active and passive immunization) or improvement in general health by nutrition and exercise.
Prevention may be targeted at the microbial agent (pathogen), the human reservoir, the portal of exit, the transmission chain, the portal of entry, and disease establishment in the new host. Pasteurization of milk, chlorination of water, anti-microbial drugs (antibiotics amf anti-viral) eradicate the agent and prevent further transmission. The human reservoir can be isolated or treated to prevent disease transmission. Transmission at the portal of exit is prevented by physical protection (mosquito nets, protective clothing, condomsm, masks, insect repellents. Transmission from the reservoir towards a new host is interrupted by isolation, hand washing, vector control, sanitation, and sexual abstinence. Transmission at the portal of entry is interrupted by use of masks, condoms, and insect repellents. Establishment of disease in the new host is prevented by immunization, health education, nutrition, health promotion, ans sexual abstinenvce.
Bacterial and viral diseases are generally immunisable whereas fungal and protozoal diseases are not. The goals of immunization are eradicating disease. More modest objectives are regional elimination of disease or control of disease by reducing morbidity and mortality. Immunization leads to both individual protection and increase of herd immunity. The minimum proportion of the population that must be immunized in order to achieve herd immunity is given by 1 – 1/R0 where R0 = basic reproductive rate. Immunization is of direct benefit to the immunized except in the case of rubella in which the offspring are the main beneficiaries. Large-scale vaccination programs result in an upward shift of the average age at infection due to the decrease in the proportion of the susceptibles being infected. In active immunisation a vaccine is given to stimulate antibody production. The vaccines are in the form of live attenuated, Dead/inactivated, Active components, and toxoids (detoxified toxin). The primary IgM antibody response is seen in 1-3 weeks. The secondary IgG antibody response appears later but is permanent. In passive immunisation an already-formed antibody eg tetanus anti-toxin is given. In some disease immunization of animal reservoirs may be done in addition to human immunization. The Expanded program on immunization (EPI), started in 1974, seeks to eliminate 6 childhood diseases: TB, diphtheria, tetanus, pertussis, polio, and measles. The effectiveness of vaccination programs is assessed based on the following factors: Effectiveness in prevention as assessed by morbidity and mortality, safety and efficacy as assessed by pre-licence vaccine trials and post licence monitoring, balance between need and risk, practicability, cost, uptake of vaccine and acceptability. Vaccine effectiveness (VE) is measured as the differences in attack rates in the vaccinated and unvacinated expressed as a proportion of the total number of the attack rate in the unvaccinated thus VE = (Incidence rate in unvaccinated – incidence rate among the vaccinated) / incidence rate in unvaccinated = 1 - RR. Field investigations relating to vaccination programs are carried out to achieve the following objectives: assessing the need for vaccination by analyzing morbidity and mortality data, pre-licence and post-licence monitoring, assessing vaccine efficacy by use of specific parameters, monitoring side effects of vaccines including the common and rare ones, assessing uptake and implementation of vaccination programs, evaluation of factors affecting vaccination programs, and costing studies The following parameters are used: disease incidence rates, immunological testing eg tuberculin test, seroconversion, and sero-prevalence. Community randomized, case control and follow-up studies can be employed in field investigations. Serological surveys can also be used to assess vaccination effectiveness. Failure of the vaccination program is indicated by lack of change in disease rates, increasing disease rates, or occurrence of disease in the vaccinated.
Immunization carries with it a relatively low risk of adverse reactions heavily outweighed by the disease preventive benefits. The rates of various adverse reactions to BCG vaccination are: disseminated infection <0.1 per 100,000; osteomyelitis <0.1-30 per 100,000; and suppurative adenitis 100-4000 per 100,000. The rates of various adverse effects to DPT immuniization are convulsions 0.3-90 per 100,000; encephalitis 0.1-3 per 100,000; brain damage 02.-0.6 per 100,000; and death 0.2 per 100,000. Comparison of adverse effects in the DPT-immunized and non-immunized children in the following table makes the case for immunization. (page 374 John M Last Public Health and Human Ecology 2nd edition Prentice Hall International, Inc.) :
Complication | Cases Per Million | |||
Birth – 6 months | 6 months – 5 years | |||
Immunized | Non-immunized | Immunized | Non-immunized | |
Hospitalization | 1060.0 | 11,098.0 | 34,048.0 | 356,566.0 |
Death | 12.5 | 130.6 | 6,529.0 | 38,787.0 |
Encephalitis | 2.4 | 25.5 | 162.0 | 87.0 |
Residual Defect | 0.8 | 8.5 | 54.0 | 29.0 |
SECONDARY PREVENTION
NON-EPIDEMIC: Non-epidemic secondary prevention consists of diagnosing and treating cases. A non-epidemic situation can be treated as a problem to be resolved. The problem must first be ascertained to exist. Relevant literature on the subject is reviewed. Next techniques of descriptive epidemiology are applied by describing the time, place, abd person characteristics of the problem. The problem is described using indicators of mortality, morbidity (incidence and prevalence), and disability. The end-result of epidemiological description is generation of hypotheses that can be tested using analytic epidemiology techniques that employ cross-sectional, case control, and follow-up study designs. In some situations experimental studies in animals or humans may be needed to answer etiological questions. The information collected must be assessed for bias and artifacts, validity, and reliability. Assessment must then be made for potential confounding effects on the purpoted etiological association. The final conclusion regarding causality is reached after considering the data using the criteria of causality: temporal sequence, strength of association, specificity, dose response, coherence, and consistency. Once the etiological relation is clear, preventive measures are undertaken. Understanding of the causal relationship and planning preventive approaches can be enriched by studying interaction or effect modification.
EPIDEMIC: In case of a community outbreak of an infectious disease, a systematic investigation is needed. The purpose of the investigation is to get information necessary for undertaking control and preventive measures. Clinical, epidemiological, microbiological, and laboratory evidence are combined to reach a conclusion on what measures to take. The processes involved in the investigation are: determining whether there is an epidemic by rapidly analysing reports of cases; confirming the diagnosis of disease using clinical and laboratory criteria; agreeing on case definition; collecting data emphasising the epidemiologic characteristics of time, place, and person; determining who is at risk of infection; and suggesting a hypothesis and testing it using available data or deciding to collect more systematic data. Practical plans of containing the epidemic are then drawn up based on conclusions from hypothesis testing. A report is written and mechanisms are set up for long-term surveillance and prevention.
TERTIARY PREVENTION
Tertiary prevention: limit chronic disability by physiotherapy, supportive care, and surgical correction of deformities. Tertiary prevention for an individual aims at convalescence, recovery to full health, and return to normal activity. Tertiary prevention for the community aims at preventing the recurrence by disinfection and reapplication of primary and secondary preventive measures to prevent new cases of the disease.
CONTROL OF DISEASE OUTBREAK
An epidemic is an emergency situation. The problem is unexpected but immediate action must be taken. Investigations, deliberations, and detailed planning must of necessity be limited. Preparation for field investigation of a disease outbreak includes the following elements: selection and training of personnel, acquiring equipment, collaboration & consultation arrangements, setting up an efficient communication system, setting up an administrative structure, identifying the leader and defining the role of each member of the team. The investigation of an outbreak comprises socio-demogarphic information and information about the infection. Socio-demographic information is age, sex, occupation, and ethnicity. Information on the infection covers: identification of the cases, places of infection using a map, number of cases per time period, the source of infection, the mode of transmission, the people at risk of infection, and predisposing factors to infection rate of infection. Analytic studies (case-control or follow-up) as well as anecdotal observations are employed. Control of the outbreak: When the causative organism is known, drug treatment is usually needed. A choice is made between static and cidal drugs; cidal drugs are preferred. Drugs must have selective toxicity in that they kill the microorganism without harming the human host. If possible, drug choice should be preceded by sensitivity testing. If not possible, a broad-spectrum drug must be used. Antibiotics can be used for known infections and also for prophyllaxis of the susceptible. Drugs can cause toxicity, hypersensitivity, or harm the normal flora. Indiscriminate mass use of antibiotics should be discouraged because it leads to primary and secondary drug resistance (mutation & selection, plasmids). Cross-resistance can occur in some cases. Antibiotic prophylaxis can be pre or post exposure. Other control approaches include quarantine, isolation, and disinfection. Post-outbreak surveillance: Serological, bacteriological, epidemiological, and clinical surveillance is carried out after the acute phase. Report of the out-break: At the end an epidemic report should be written showing the following main elements: causative organism, routes of transmission, epidemic curve, geographical distribution, clinical presentation, reason for the epidemic, and control measures used. The report serves the purposes of basic documentation for further action; record of what was done; medico-legal considerations; contribution to scientific knowledge; and as a teaching tool.
BREAKING THE TRANSMISSION CYCLE BY TYPE OF DISEASE
The transmission cycle of respiratory infections is broken by reducing direct contact with the infectious source, isolation of serious infections, chemoprophyllaxis, and face masks. The transmission cycle of gastro-intestinal infections is by sanitation measures, fod hygiene, fly control, and personal hygiene. The transmission cycle of sexually transmitted diseases is broken by avoiding promiscuity and genital hygiene. The transmission cycle of vectorborne diseases is broken by chemoprophyllaxis and vector control (destroying breeding sites, prevent vector-host contact or access, and use of pesticides. The transmission cycle of zoonoses is by control of animal hosts. Immunization where applicable is a general measure of breaking the transmission cycle.
UNIT 7.2
VIRUSES
Learning Objectives
- Incidence, prevalence, and risk factors of common viral infections
- Routes of transmission and methods of prevention
Key Words and Terms
- Transmission, feco-oral
- Transmission, air borne
- Transmission, parenteral
- Infection, endemic
- Infection, sporadic
- Infection, epidemic
- Infection, pandemic
- Infection, cyclic
- Infection, seasonal
- Antigenic drift
· Carrier
UNIT OUTLINE
7.2.1 VIRAL INFECTIONS: FECO ORAL
A. HAV
B. COCKSACKIE VIRUS
C. ECHO VIRUS
D. ROTA VIRUS
E. LASSA VIRUS
7.2.2 VIRAL INFECTIONS: AIR-BORNE
A. HSV 1
B. VZ
C. EBV
D. RHINOVIRUS
E. MEASLES
F. MUMPS
G. RUBELLA
H. INFLUENZA
7.2.3 VIRAL INFECTIONS: VECTOR-BORNE
A. YELLOW FEVER
B. DENGUE
C. JE
7.2.4 VIRAL INFECTIONS: PARENTERAL
A. HSV 2
B. CMV
C. HBV
D. HDV
E. HIV
7.2.5 VIRAL INFECTIONS: OTHERS
A. RABIES
7.2.1 VIRAL INFECTIONS: FECO ORAL
A. HAV
HAV infection is endemic, sporadic, and epidemic. There are no carriers. Travelers abroad are at higher risk. HEV is common in the Indian sub-continent. Pregnancy is associated with higher risk. Polio causes myositis, brain degeneration, and paralysis. It is endemic in less developed countries. It is commonest in both males and females at <5yr. It is rare in developed countries.
B. COCKSACKIE VIRUS
Cocksackie infection occurs in an epidemic form.
C. ECHO VIRUS
ECHO virus causes meningitis, and enteritis. It has world-wide distribution. Low SES. And & childhood are associated with higher risk.
D. ROTA VIRUS
Rota-virus causes childhood enteritis. It has world-wide distribution. It is endemic and epidemic in the tropics. Children aged 6-24 months are at higher risk.
E. LASSA VIRUS
Lassa virus causes Lassa fever. It was first described in Nigeria
7.2.2 VIRAL INFECTIONS: AIR-BORNE
A. HSV 1
HSV 1 infection is more common in low SES and crowded conditions.
B. VZ
VZ causes shingles/chicken pox with peak incidence is at ages 2-6 years. It is severe in infants and the immune compromised. Shingles in the elderly is reactivation of primary childhood infection.
C. EBV
EBV causes infectious mononucleosis. EBV infection LDC it is an asymptomatic childhood infection. In industrialised countries it is a symptomatic disease of young adults called infectious mononucleosis. Influenza virus causes respiratory infection. It is seasonal, endemic, and epidemic. It manifests the phenomenon of antigenc drift. The elderly are at higher risk.
D. RHINOVIRUS
Rhinovirus causes common cold.
E. MEASLES
Measles virus causes measles. It is epidemic and endemic. Low SES and crowding are high risk factors. In LDC it is a disease of childhood. Adult infections occur in industrialised countries.
F. MUMPS
Mumps virus: causes mumps. It is common in childhood. It may cause sterility due to oochitis.
G. RUBELLA
Rubella virus: causes the rubella syndrome. It is endemic. Pregnancy and childhood are associated with higher risk
INFLUENZA
Influenza infection illustrates the eoidemicity of viral diseases. Several influenza pandemics have been described. The 1732-1733 pandemic was world-wide and caused death rates 2-3 times above normal levels in European cities. The 1781-1782 pandemic in Europe, North America, China , and India China Russia affected Europe, North America, and South America . The 1857-1858 pandemic started in Panama and affected North America, Central America, and South America and also spread to Europe . The 1889-1890 Asian influenza pandemic started in Russia China South-east Asia and caused high morbidity and moderate mortality. The 1968-1969 Hong Kong influenza had lower mortality that the 1957 pandemic and was the first epidemic in which vaccination might have been efficacious.( page 129 John M Last: Public Health and Human Ecology 2nd edition Prentice Hall International, Inc.)
7.2.3 VIRAL INFECTIONS: VECTOR-BORNE
A. YELLOW FEVER
Yellow fever virus causes yellow fever. Focal outbreaks occur in Africa, S. America, & the Caribbean . It is not found in Asia . Incidence is equal in males and females. All races and all ages are affected.
B. DENGUE
Dengue virus causes dengue fever that can be severe in its hemorrhagic form. It is common in the tropics & subtropics. It is cyclic and seasonal. Incidence in males and females is equal. All ages are affected.
C. JE
Flavivirus: causes Japanese encephalitis. JE is epidemic in Japan , Taiwan , and Korea
7.2.4 VIRAL INFECTIONS: PARENTERAL
A. HSV 2
HSV 2 infection is at high in the high-risk groups of the promiscuous and the homosexuals. B. CMV
CMV infection is endemic. The incidence rate of infection rises with age. Risk is higher in infants and the imune compromised.
C. HBV
HBV infection causes hepatitis, a world-wide condition. The chronic carrier rate is 30% in the Middle East, the Far East, and sub-Saharan Africa . High risk groups are: homosexuals, Iv drug users, blood transfusion workers, health care personnel, and prostitutes. HBV is associated with cirrhosis and hapato-cellular carcinoma. HCV occurs world-wide. The carrier rate varies: Europe 0.2%, Far East 5%, and Middle-east 1-2%. Intravenous drug users and dialysis patients are at higher risk of infection.
D. HDV
HDV infection occurs world-wide. It is endemic in the mediteranean, N Europe, and USA
E. HIV
HIV causes AIDS. AIDS occurs world-wide. It is a current epidemic. Homosexuals, promiscuous heterosexuals, iv drug users, blood transfusion workers, health care workers are at higher risk
7.2.5 VIRAL INFECTIONS: OTHERS
A. RABIES
Rabies virus causes rabies. Its occurrence is endemic, epidemic, and sporadic. It has world-wide distribution especially in Asia, Africa, Central and South America . Veterinarians are at high risk of infection.
UNIT 7.3
PROKARYOTES
Learning Objectives
- Incidence, prevalence, and risk factors of common viral infections
- Routes of transmission and methods of prevention
Key Words and Terms
- Transmission, feco-oral
- Transmission, air borne
- Transmission, parenteral
- Infection, endemic
- Infection, sporadic
- Infection, epidemic
- Infection, pandemic
- Infection, cyclic
- Infection, seasonal
- Antigenic drift
- Carrier
UNIT OUTLINE
7.3.1 BACTERIA INFECTIONS: FECO-ORAL
A. KLEBSIELLA
B. SHIGELLA
C. E COLI
D. SALMONELLA
E. CHOLERA
F. H PYLORI
G. CLOSTRIDIUM
H. COMPYLOBACTER
7.3.2 BACTERIAL INFECTIONS: DROPLET SPREAD
A. BORDETELLA
B. DIPHTHERIA
C. H INFLUENZAE
D. STREPROCOCCUS
E. TUBERCULOSIS
F. LEPROSY
7.3.3 BACTERIAL INFECTIONS: SEXUALLY TRANSMITTED
A. GONORRHOEA
B. SYPHILIS
7.3.4 BACTERIAL INFECTIONS: OTHERS
A. BRUCELLA
B. PLAGUE
C. ANTHRAX
D. TETANUS
E. LEPTOSPIROSIS
7.3.5 CHLAMYDIAL & RICKETTSIAL INFECTIONS
A. RICHETSIA
B. TRACHOMA
C. Q FEVER
D. SPOTTED FEVER
7.3.1 BACTERIA INFECTIONS: FECO-ORAL
A. KLEBSIELLA
K. pneumonae causes diarrhoea & respiratory tract infection.
B. SHIGELLA
Shigella spp, world-wide in distribution with common epidemics, cause shigellosis.
C. E COLI
E. coli causes gastro-intestinal and urinary tract infection. It is world-wide.
D. SALMONELLA
Patients in hospitals and neonates are at higher risk Salmonella spp causes salmonellosis. It is distributed world-wide. It can occur as endemic or epidemic disease. It can also occur as a disease outbreak.
E. CHOLERA
V. cholerae causes cholera. It is endemic in South Asia especially in the rainy season. It is endemic in children and epidemic for all ages.
F. H PYLORI
H. pylori causes peptic ulcer. The prevalence of H.pylori infection is 88% for gastric and duodenal ulcer patients. The prevalence increases with age.
G. CLOSTRIDIUM
Cl. botulinum is the cause of botulism.
H. COMPYLOBACTER
Compylobacter spp causes enteritis. It is world-wide. It affects infants, young children, and young adults.
7.3.2 BACTERIAL INFECTIONS: DROPLET SPREAD
A. BORDETELLA
B. pertussis causes pertussis and mental retardation. It is endemic and epidemic. Children below 5yr are at higher risk. Whooping cough caused by Bordetella Pertussis has been declining in England and Wales
B. DIPHTHERIA
C. diphtheriae is the cause of diphtheria. It also causes myocarditis and neurological complications. The incidence rate is decreasing with mass vaccination. Risk is higher in children and crowded living conditions.
C. H INFLUENZAE
H. influenzae causes URTI and meningitis. It is world-wide. Children under 5 yr and immunecompromised children are at high risk.
D. STREPROCOCCUS
S pyogenes causes URTI. It is world-wide. It has a seasonal distribution. S agalactae causes neonatal Infection. S fecalis causes UTI. S pneumonae causes pneumoniaa, URTI, and meningitis. It is world-wide. It is both sporadic and epidemic. S viridans causes endocarditis. S aureus & S epidermidis cause skin infections, pneumonia, and food infection. They occur world-wide in sporadic and epidemic forms.
E. TUBERCULOSIS
M. tuberculosis causes tuberculosis. It is world-wide. It has a bi-modal distribution with peak incidences at ages 15-44 and 60+. Improved living conditions in Europe in the second half of the 19th century G resulted in the fall of tuberculosis rates in the general population from about 3000 deaths per million of general population to below 100 per million in 1960G. The general trend of falling tuberculosis death rates was not affected in any drastic way by the discovery of anti-tuberculosis chemotherapy in the 1940s (page 130 John M Last: Public Health and Human Ecology. 2nd edition. Prentice Hall International, Inc ? year). The recent rise of incidence is due to immuno-incompetence caused by HIV infection. The elderly, medical workers, and alcoholics are at higher risk of TB infection.
F. LEPROSY
M. leprae causes leprosy, a disabling condition. It is common in the topics & sub-tropics. Male cases are more than female cases. N. meningitidis causes meningitis. The epidemiology is poorly understood. It is endemic and sporadic and is commonest in dry hot countries. It displays strong seasonality.
7.3.3 BACTERIAL INFECTIONS: SEXUALLY TRANSMITTED
A. GONORRHOEA
N. gonorrhoae causes gonorrhoea. It is world-wide. Incidence is rising. It is generally asymptomatic in females. It is associated with the following gynecological complications: cervicitis, pelvic inflammatory disease, ectopic pregnancy, chronic pelvic pain, and infertility. It is responsible for urethritis, epididymitis, and strictures in males. It causes the following complications in infants and newborns: ophthalmia neonatorum, corneal ulceration leading to blindness and low vision, and low birth weight.
B. SYPHILIS
Tr. Pallidum causes syphilis. Homosexuals and medical workers are at high risk. Syphilis manifests as the following clinical syndromes: low birth weight, congenital syphilis, secondary syphilis, and tertiary syphilis (cardio-vascular complications, gummas, and neurosyphilis).
7.3.4 BACTERIAL INFECTIONS: OTHERS
A. BRUCELLA
Brucella spp is the cause of brucellosis. It is found more in males than females. Farm workers are at higher risk.
B. PLAGUE
Y. pestis is the cause of plague. The disease is endemic in Africa, Asia, S. America, and Southern USA . Medical workers are at higher risk.
C. ANTHRAX
B. anthracis causes anthrax (cutaneous & pulmonary). It is rare in industrialised countries; common in LDC. It is an occupational disease among persons working with animals or animal products.
D. TETANUS
Cl. tetani causes tetanus. It is rare in industrialised countries or where immunisation is carried out. It occurs in an endemic form. Farmers, i.v. drug users, and newborns are at higher risk.
E. LEPTOSPIROSIS
Leptospira spp causes leptospirosis. It is found more in rural areas. Hospital staff, estate workers, and school children are at higher risk.
7.3.5 CHLAMYDIAL & RICKETTSIAL INFECTIONS
A. RICHETSIA
Rickettsia spp causes typhus. It occurs in both endemic and epidemic forms. It is commonest in the mountains of Ethiopia , S. America, and the Himalayas . R. tsutsumagushi causes scrub typhus. It is found in Asia . Farmers are at higher risk.
B. TRACHOMA
Cl. trichomatis causes ophthalmia neonatorum, neonatal pneumonia, low birth weight, and trachoma. Trachoma, which is corneal ulceration common in Africa & the Mediterranean region, leads to blindness and low vision both in neonates and adults. Cl. trichomatis causes nonspecific genital infection (pelvic inflammatory disease, cervicitis, ectopic pregnancy, tubo-ovarian mass, chronic pelvic pain, infertility, urethritis, epididymitis, and urethral striucture). It is found in Africa, Asia , and S.America.
C. Q FEVER
C burnetti causes Q fever.
D. SPOTTED FEVER
R Rickettsi causes spotted fever. It is found in the eastern USA , S America, and Africa . People in tick infested areas are at high risk.
UNIT 7.4
EUKARYOTES
Learning Objectives
- Incidence, prevalence, and risk factors of common viral infections
- Routes of transmission and methods of prevention
Key Words and Terms
- Transmission, feco-oral
- Transmission, air borne
- Transmission, parenteral
- Infection, endemic
- Infection, sporadic
- Infection, epidemic
- Infection, pandemic
- Infection, cyclic
- Infection, seasonal
- Antigenic drift
- Carrier
UNIT OUTLINE
7.4.1 PROTOZOAL INFECTIONS
A. GIARDIASIS
B. TRICHOMONIASIS
C. TRYPANASOMIASIS
D. AMEBIASIS
E. MALARIA
7.4.2 HELMINTHIC INFESTATIONS
A. ASCARIASIS
B. CLONORCHIOSIS
C. DRANCUNCULOSIS
D. DRANCUCULOSIS
D. FILARIASIS
E. HOOKWORM DISEASE
F. LOAIASIS
G. ONCHOCERCIASIS
H. SCHISTOSOMIASIS
I. STRONGYLOIDOSIS
J. TENIASIS
H. TRICHURIASIS
I. TOXICARIASIS
J. TRICHINOSIS
K. FASCIOLASIS
L. HYDATID DISEASE
M. ENTEROBIOSIS
7.4.3 FUNGAL INFECTIONS
A. TINEA
7.4.1 PROTOZOAL INFECTIONS
A. GIARDIASIS
G. lamblia causes giardiasis. It has world-wide distribution being most in the tropics. It occurs in both endemic and epidemic forms. Children and male homosexuals are at higher risk of infection.
B. TRICHOMONIASIS
T. vaginalis: causes trichomoniasis. It is world-wide in distribution.
C. TRYPANASOMIASIS
T. brucei: causes African trypanasomiasis. It is found in East and Central Africa . Living in an endemic area is a high-risk factor. T. cruzi: causes American trypanasomiasis common in Central and South America . Children below 10 years and persons living in poor housing are at high risk. It is associated with the following complications: cardiomyopathies, congestive cardiac failure, and megaviscera.
D. AMEBIASIS
E. histolytica causes amebiasis. It is world-wide and endemic. Low sanitation is a risk factor.
E. MALARIA
Plasmodium spp: causes malaria. It is common in the tropical and sub-tropical regions of Africa, Asia, and Latin America . Its incidence is more in children. It is more severe in pregnancy due to the associated immune incompetence. It is associated with anemia, neurological sequelae, and renal complications. T. gondi causes toxoplasmosis which manifests as visceral leishmaniasis (kala-azar) or cutaneous leishmaniasis. It is world-wide. 20-40% of adults in Britain Mediterranean , and Middle Asia. It occurs in endemic, epidemic, and sporadic forms. Incidence in males is equal to that in females. It affects all ages. P carinii : causes interstitial pneumonitis. It occurs world-wide. Low immunity in AIDS is a risk factor.
7.4.2 HELMINTHIC INFESTATIONS
A. ASCARIASIS
A. Lumbricoides causes ascariasis that can cause intestinal obstruction. It occurs world-wide and is very common. Incidence is highest in the tropics and sub-tropics. Higher risk is found in poor sanitation, farmers, and children.
B. CLONORCHIOSIS
Cl. sinensis: causes clonorchiosis. It is commonest in Asia .
C. DRANCUNCULOSIS
D. medinensis causes dracunculosis. It is common in Africa , the Middle-east, and the Indian sub-continent.
D. FILARIASIS
W. bancriofti, B.malayi, and B timori: cause filariasis which manifests as lymphedema and hydrocele. These are diseases of the tropical and sub-tropical regions of S. America, Africa, Asia , and the Pacific islands. They are more common in the rural areas. B malayi is found in Asia only.
E. HOOKWORM DISEASE
A duodenale & N americanus: cause hookworm disease and anemia. They are world-wide and are endemic. All ages are affected with higher incidence in children aged 5-15 years. The high risk factors are: farming, rural living, and childhood.
F. LOAIASIS
Loa loa causes loaiasis (blindness, low vision, and itching). It is found in the topical rain forest of West and Central Africa .
G. ONCHOCERCIASIS
O. volvulus: causes onchocerciasis. It is found in equatorial Africa, Central and South America . Living near water is a high-risk factor.
H. SCHISTOSOMIASIS
Schistosoma spp: Schistosomiasis is a disease of the tropical and subtropical regions of Africa, Asia , and S.America. S. japonicum is found only in Asia .
I. STRONGYLOIDOSIS
S. stercoralis: causes strongyloidosis. It occurs world-wide.
J. TENIASIS
T.saginata & T.solium cause cycticercosis. It is found world-wide especially in Asia, Africa, the Middle- east, and South America .
H. TRICHURIASIS
T. .trichuria: causes trichuriasis (diarrhoea and anal pruritis). It is found world-wide.
I. TOXICARIASIS
T.cani & T. cati: cause toxicariasis. They are found world-wide. Working with dogs is a high risk factor.
J. TRICHINOSIS
T spiralis: causes trichinosis. It is found world wide being more common in the Americas , Asia, Africa , and the Artic.
K. FASCIOLASIS
F. hepatica causes fasciolasis.
L. HYDATID DISEASE
E granulosus: causes hydatid disease. It is endemic in Turkey , the Middle-east, Kenya , and S America .
M. ENTEROBIOSIS
E vermicularis: causes enterobiosis. It is world-wide. High prevalence in children, institutions, & families
7.4.3 FUNGAL INFECTIONS
A. TINEA
Tinea cruris causes jock itch. Tinea pedis causes athlete’s foot.
UNIT 7.5
EMERGING and RE-EMERGING INFECTIONS
Learning Objectives
- Incidence trends of emerging and re-emerging communicable diseases
- Life style and environmental factors related to emerging communicable diseases
Key Words and Terms
- New And Old Diseases
- Reemerging Infectious Diseases
- Socio-Demographic Factors
- Environmental Factors
- Medical Technology
- Nosocomial Infections
- Traditional Sexually Transmitted Diseases
- Hiv/Aids
- Marburgh/Ebola Virus
- Swine Flu
- Lassa Fever
- Dengue Fever
- Hanta Virus
- Hepatitis
- Rift Valley
- Yellow Fever
- Streptococcus
- Streptococcus Group A Is An Invasive Necrotizing ‘Flesh-Eating’ Bacterium
- The Toxic Shock Syndrome
- Toxigenic Vibrio
- Brazilian Purpuric Fever
- Helicobacter Pylori
- Tuberculosis
- Malaria
- Lyme Disease
- Legionnaire’s Disease
- Opportunistic Infections
UNIT OUTLINE
7.5.1 OVER VIEW
A. New and Old Diseases
B. Socio-Demographic Factors
C. Environmental Factors
D. Medical Technology
E. Hospital Infections
7.5.2 SEXUALLY TRANSMITTED DISEASES
A. Traditional Sexually Transmitted Diseases
B. HIV/AIDS
7.5.3 VIRAL DISEASES
A. Marburgh/Ebola Virus
B. Swine Flu
C. Lassa Fever
D. Dengue Fever
E. Hanta Virus
F. Hepatitis
G. Rift Valley
H. Yellow Fever
7.5.4 BACTERIAL DISEASES
A. Streptococcus
B. Staphylococcus
C. Enteropathogens
D. Hemophilus
E. E. H. Pylori
F. Tuberculosis
7.5.5 PARASITIC DISEASES:
A. Malaria
B. Lyme Disease
C. Legionnaire’s Disease
D. Opportunistic Infections
E. Cryptosporidium Spp, Cyclospora Spp
F. The Esinophilia-Myalgian Syndrome
7.5.1 OVER VIEW
A. NEW AND OLD DISEASES
The reemergence of infectious diseases in the developed countries requires an explanation because they had been falling over most of the 20th century. The causes may be socio-demographic, lifestyle or human behavior, environmental, and medical technology. According to the World Health Report of 1996, diseases and the associated problems may be old or new. Some diseases are old diseases and are old problems like measles, polio, leprosy, tetanus, hepatitis, and typhoid. Some diseases are old but are new problems for example the rising incidence of tuberculosis, malaria, and dengue due to drug and insecticide resistance. Ebola, HIV, and hantavirus infection are new diseases with new pathogens.
B. SOCIO-DEMOGRAPHIC FACTORS
Demographic changes (aging, migration), wide scale commercial and tourist travel, increasing crowding especially in the large urban areas, behavioral and lifestyle changes are factors contributing to emerging infectious diseases.
C. ENVIRONMENTAL FACTORS
Another potential contributing factor to emerging diseases is global environmental change manifesting as global warming, climate change, rising sea levels, heat waves, and ozone depletion. Climatic change results in disturbances in the ecosystem leading to favoring growth and transmission of old and new pathogens. Resource depletion will affect health directly due to shortage of fresh water and food supplies and indirectly favor development of disease. Environmental pollution in industrialized regions of the world will also have an impact on health.
D. MEDICAL TECHNOLOGY
Immune suppression for organ transplantation,
E. HOSPITAL INFECTIONS
Incidence and prevalence of nosocomial infections: Nosocomial infections are defined as those acquired in the hospital. Bacterial nosocomial infections occur world-wide. Nosocomial infections occur in 6% of admitted patients in the UK US
Sources and causes of infection: Infection may be from the patients, the health care providers, or the environment. Patients are the commonest reservoir of infection. Infective waste especially from the laboratories may be sources of contamination. Some infection may be acquired from the food or water given to patients. The organisms involved are usually: E.coli, P. eruginosa, enterobacter spp, proteus spp, provedentia spp, S.aureus, and enterococcal group B. Many hospital infections are opportunistic. Patients with immunosuppression either due to their original disease or chemotherapy are susceptible to infection by organisms that normally do not cause systemic disease like fungi or protozoa like P. carinii. Cancer patients on treatment and transplantation patients usually suffer from such infections. Medical or surgical procedures introduce infective organisms into the body for example: catheterization and renal dialysis. Surgical wounds are liable to infection. Pressure ulcers may be complictad by infection. Pneumonia may result from ventilation.
Pathology: Nosocomial infections commonly affect the urinary tract, surgical wounds, and the respiratory tract. Primary bacteremia is a serious but rare consequence. Infecting organisms are often drug-resistant.
Epidemiological studies: Epidemiological studies of hospital infections are prevalence studies, incidence studies, or investigations of a disease outbreak. Investigation of disease outbreak in a hospital starts with a determination that there is indeed an outbreak. The diagnosis is confirmed. A case definition is developed to enable counting the cases. The outbreak is described in terms of time, place, and persons involved. A determination is then made of who else is at risk. Control measures are put in place. Hypotheses about the spread of the disease are developed and are tested in a more systematic study. A written report is made. All through care must be taken to document properly in preparation for possible litigation on the basis of malpractice.
Control: Primary prevention is by hand-washing, cleaning, disinfecting, sterilisation of equipment, microbiological sampling, proper disposal of infectious waste, good housekeeping, and laundry, continuous surveillance by a hospital epidemiologist by sampling for bacteria and monitoring drug resistance, and prophylactic treatment for those at high risk. Secondary prevention is by Vigorous treatment of the infection preferably after culture and sensitivity tests. Surveillance is achieved by continuous sampling for bacteria and assessing drug resistance. The hospital clinical data base can also be used to identify profiles of infections that may point to a nosocomial source. The computer can be programmed to detect abnormal patterns that call for closer inspection.
7.5.2 SEXUALLY TRANSMITTED DISEASES
A. TRADITIONAL SEXUALLY TRANSMITTED DISEASES
Breakdown of traditional society and emergence of liberal ideas about sexual relations is behind the increase of STD. The traditional STDs are syphilis, gonorrhoea, and chanchroid. New diseases are chlamydia, genital warts, trichomonas, scabies, peduculosis, genital herpes, vaginal candidiasis, E. histolytica infection, G. lamblia, HVA, HBV, HCV, and HIV. STDs have serious complications such as PID, menstrual pain, coital pain, and infertility. Data on STDs is inadequate because of incomplete notification. Diagnostic criteria are not uniform. Data available relates to cases and not patients. STDs are asymptomatic especially in women. Approaches used are sentinel clinics and adhoc surveys. Population-based serological surveys are possible for HSV-2. Health education does not seem to be very effective in the prevention of STDs. Use of condoms by commercial sex workers is effective in decreasing STD incidence.
B. HIV/AIDS
Acquired Immunodeficiency syndrome appeared in 1981,
Agent: The HIV 1 virus was isolated by Montaignier et al. in 1983 at the Pasteur Institute in Paris West Africa . HIV attaches to the CD4+ lymphocytes which are depleted as the infection progresses.
Epidemiology: HIV was first diagnosed in 1981 in homosexuals. It was found in intravenous drug users and blood product recipients in 1982. The epidemiology of HIV closely resembles that of other STDs. Humans are the only reservoir. HIV is transmitted by semen, blood, vaginal and cervical secretions. The portal of entry and exit is the uro-genital tract during sexual transmission. HIV transmission occurs in both homosexual and heterosexual contacts. The receptive homosexual partner is at a higher risk of getting the infection. Direct transmission occurs when contaminated syringe needles are shared by iv drug users, the perinatal period, breast milk, transfusion of blood and blood products, insemination with donated semen, transplantation of organs and tissues. The risk of transmission in blood transfusion is virtually 100%. Health care workers can transmit or get infection during medical procedures. Determining community prevalence of HIV infection is not easy due to the long incubation period of the disease. Community surveys can not be reliable because many people would refuse to take the HIV tests. Seroprevalence surveys based on persons in the health care system are not reliable because they are not representative. Blood donors are a select group of persons with no HIV risk factors. Hospital patients tend to be generally older than other members of the community; they also overrepresent young women because of obstetric-related admissions. Women attending the ante-natal clinics are also not a representative population because the infertile women are more likely to have a higher risk for HIV infection.
Natural history: The natural history of HIV can be studied in both the sexually transmitted and the non sexually transmitted disease. In the sexually transmitted disease in which one partner is infected and the other is not, the non infected partner can be followed to see disease development. This can be related to coital frequency and the risk per coitus can be computed. Bias can occur because the partners start using protective methods once they discover that one of them is infected. For the non sexually transmitted disease, cohort studies can be done for health workers exposed by pricks or post delivery study of babies of infected mothers. The time at infection is difficult to ascertain in the sexually transmitted disease. Time at infection can be ascertained in cases due to transmission by blood transfusion with care being taken to eliminate the bias that arises due to those exposed but develop symptoms late. Antibodies appear 3-6 months after exposure. The incubation period ranges 2-15 years with a median of 10 years. The maximum of the incubation period is not known for certain because this is a young epidemic that is still evolving. The ratio of CD4+ to CD8+ lymphocytes can be used as a surrogate measure of incubation time. The HIV antigen disappears a short time after infection. Symptoms appear 8-10 years later usually when CD4+ lymphocytes are depleted. AIDS is diagnosed after another 2 years. Death usually ensues 5 years of AIDS diagnosis.
Diagnosis: Sero-epidemiological studies depend on ELIZA followed by Western Blot confirmation. There is a window of 3 weeks to 3 months between infection and appearance of antibodies. The clinical manifestations are varied and consist of the seroconversion syndrome, persistent generalized lymphadenopathy, indicator diseases of HIV infection (candidiasis, cryptosporodiosis, CMV infection, HSV infection, P. carinii pneumonia, Kaposi sarcoma, reactivation of primary TB, and mycobacterium avium infecton), encephalopathy and other psychiatric symptoms, and the wasting slim disease. Frank AIDS is a late manifestation.
Control and prevention: Anti-retroviral drug treatment of the infected slows pathogen multiplication and delays appearance of AIDS. The infected must abstain from sexual contact. Extra care must be taken during medical procedures. Universal precautions are disease prevention guidelines for those who may come into contact with body fluids of persons infected with HIV. Primary prevention consists of safe sex (monogamy or condom use), voluntary testing and contact tracing, safe blood supplies with use of antigen screening during the window between infection and appearance of antibodies, safe organ donation programs, precautions in medical facilities, and development of a vaccine.
Economic impact: HIV infection has a demographic impact because it affects young adults. Mathematical models are used to predict the future course of the disease. These may be simple statistical extrapolation or may be more sophisticated process models.
7.5.3 VIRAL DISEASES
A. MARBURGH/EBOLA VIRUS
The Marburgh virus disease was first recognized in Yugoslavia and Germany when people fell ill after contact with monkeys imported from Uganda US by importation of monkeys from Africa .
B. SWINE FLU
The A swine flu epidemic was recognized in 1976.
C. LASSA FEVER
Lassa fever spread is favored by urbanization favoring rident exposure in the homes.
D. DENGUE FEVER
Travel, migration, and urbanization contribute to spread of dengue fever and dengue hemorrhagic fever.
E. HANTA VIRUS
Hanta viruses are spreading because of ecological and environmental changes that increase contact with rodents. The Hantavirus pulmonary syndrome due to hanta virus associated with contaminated droppings of deer mice appeared in 1993
F. HEPATITIS
Hepatitis B and C are spreading due to transfusion, organ transplantation, intravenous drug abuse, and sexual transmission.
G. RIFT VALLEY
Rift valley fever transmission is favored by dam building, agriculture, and irrigation.
H. YELLOW FEVER
Yellow fever is being transmitted in new areas because of conditions that favor mosquitoes. (Infectioius Diseases: Submerging and Emerging in Textbook of International Health 2nd edition p 480-481).
7.5.4 BACTERIAL DISEASES
A. STREPTOCOCCUS
Streptococcus group A is an invasive necrotizing ‘flesh-eating’ bacterium whose increased transmission is not understood.
B. STAPHYLOCOCCUS
The toxic shock syndrome is due to infection of ultra absorbent tampons by Staphylococcus aureus. the toxic shock syndrome due to a S. aureus toxin apeared in 1980,
C. ENTEROPATHOGENS
Shigella spp
Giardia
Food borne infections (eg E coli)
Toxigenix vibrio: Cholera transmission is due to poor sanitation and introduction of new strains (such as O139) due to travel. The hemolytic uremic syndrome is due to mass food processing technology that allows Escheria coli O157:H7 to contaminate meat.
D. HEMOPHILUS
Brazilian purpuric fever is due to a new strain of Hemophilus Influenzae.
E. H. PYLORI
Helicobacter Pylori is probably not a new disease but has just been recognized as an association with gastric ulcers and other gastro-intestinal disorders. (Infectioius Diseases: Submerging and Emerging in Textbook of International Health 2nd edition p 480-481)
F. TUBERCULOSIS
The decline of TB incidence in Europe and America
Incidence is assessed by positive sputum smear and skin tests. Prevalence is from sputum smears. Additional information is obtained from TB notifications and mortality data. Incidence of TB has increased in parellel with increase of HIV. Skin testing for TB may be false negative due to anergy induced by HIV infection. The Community Infection Ratio (CIR) is computed as [(prevalence in controls) / (1 – prevalence in controls)] / [(prevalence in contacts) / (1 – prevalence in contacts)]. A high CIR indicates a community source of infection. A low CIR indicates household sources of infection.
Control of TB is achieved by contact tracing, chemoprophyllaxis, and adherence to treatment schedules. Direct observed therapy (DOT) helps in ensuring treatment compliance. Shorter drug regimens also ensure that the problem of non-compliance does not arise.
Prevention of TB is achieved by overall improvement in nutrition, social and environmental conditions, and alleviation of poverty. Primary prevention is based on BCG vaccination and chemoprophylaxis with INH which prevents reactivation of latent TB. Secondary prevention is treatment of multi-drug resistant conditions.
7.5.5 PARASITIC DISEASES:
A. MALARIA
Malaria is spreading due to increasing travel and migration. Schistosomiasis is spreading due to dam building
B. LYME DISEASE
Among emerging infectious diseases are: Lyme disease due to a spirochete called borrelia burgdorferi appeared in 1975. Lyme disease, due to Borrelia burgdorferi, is due to reforestation around homes that favors the tick vector and the deer, a secondary reservoir host
C. LEGIONNAIRE’S DISEASE
Legionnaire’s disease due to a small infectious agent spread via air-conditioning systems appeared in 1976. Legionella (Legionnaire’s disease) is due to biofilms that form on water tanks and plumbing favoring growth of the causative organisms.
D. Opportunistic infections
p. carinii, cryptococcus spp
E. Cryptosporidium spp, Cyclospora spp
Cryptosporidium spp, Cyclospora spp and other water-borne pathogens are due to contaminated surface water and improper water purification.
the esinophilia-myalgiansyndrome due to toxic contaminants associated with the use of alpha-tryptophan appeared in 1989 (Infectioius Diseases: Submerging and Emerging in Textbook of International Health 2nd edition p 480-481).