NI's Drum lab is the best VST I have found to program drums. It has different samples for different velocities, you can set the mic to be far or close, put fx on it, etc. I would make a drum break with it, record the audio and chop it up.

means of infection
Any disease that is able to spread among the community may for normal intents be regarded as infectious. In its accepted sense, an infectious disease is one which travels through the general environment as it passes from one person to another. For instance, the disease could be transmitted by airborne droplets, or through contaminated water.

Transfer may also be effected via clothes, bedding, domestic utensils, or anything else that has been in contact with a victim. Items which assist disease transmission are called fomites (singular: fomes, Latin for touchwood). Diseases which spread as a result of direct personal contact are properly termed contagious.

A few diseases require the involvement of an intermediate animate agent in order to spread. These agents are known as vectors (Latin vectus, one who carries) and are represented by external parasites which feed from the human body, such as fleas, lice, and mosquitoes. In almost all situations, the elimination of the parasite will prevent the disease from spreading.

disease organisms
For an infectious disease to begin its harmful effects on the individual, no matter how it is spread through the community, it needs to be introduced into the body’s system by a micro-organism. Not all micro-organisms are deleterious to mankind. Those that are harmful are called pathogens. The most prolific pathogens are represented by three main groups.

1. bacteria (singular: bacterium)
These are self-contained, free-living, relatively large entities by microscopic standards. Bacteria, or ‘germs’, take in regular nourishment and excrete waste products, which are often poisonous to the host.

In general, bacteria do not penetrate the actual cells of the host’s body and are consequently described as being extracellular. To reproduce, most of them grow a little longer or wider and split into two. This process of division, called binary fission, may take place as rapidly as every twenty minutes for certain bacteria under ideal conditions – a millionfold increase in less than seven hours.

Bacteria are usually subdivided under headings according to their shape. Of the types that appear in this guide, bacilli (singular: bacillus) are rod-like and straight, spirochaeta (singular: spirochaete) are long, slender, and spirally coiled; streptococci (singular: streptococcus) are spherical and tend to grow in chains; staphylococci (singular: staphylococcus) grow in ‘bunches of grapes’; and vibrios are curved.

2. viruses
Considerably smaller than any bacterium, a virus is rather like an encoded chemical, operating only when certain conditions are available. It cannot reproduce on its own. Instead, it ‘hijacks’ a cell belonging to the body of its host and modifies the cell’s reproductive mechanism so that the cell produces viruses in place of new cells. Because of this strategy, viruses are described as being intracellular. The cell’s original function is usually destroyed in the process.

3. rickettsiae (singular: rickettsia)
Named after Dr Howard Taylor Ricketts, the American pathologist who first identified the organism, these are not to be confused with rickets, a condition caused by a lack of vitamin D. Although actually bacteria, rickettsiae are perhaps easier thought of as representing a half-way stage between viruses and bacteria. It is possible that the rickettsiae were originally similar to bacteria in form before evolving and adopting the somewhat more secure intracellular strategy of viruses.

Besides bacteria, viruses, and rickettsiae, there are other organisms capable of pathogenic activity. The only type that is pertinent to this guide are the protozoa (singular: protozoon, sometimes protozoan). The protozoa consist of a single cell and represent the lowest division of the animal kingdom. Although larger that bacteria, they are nevertheless microscopic.

immunity
The subject of immunity to disease is exceedingly complex and has by no means reached a conclusive stage of understanding.

Generally speaking, the term ‘immunity’ implies a threshold below which an individual will be little, if at all, affected by a disease organism, and above which he or she will suffer and possibly die. In practice, an individual’s threshold can shift quite markedly and sometimes suddenly under the influence of any number of factors. These might be age, diet, level of nourishment, environment, injury, tiredness, mental stress (including that emanating from the fear of the disease itself), or the effects of another disease.

Moreover, an individual might be exposed briefly to a few organisms or repeatedly to a number so vast that even the most healthy body is overwhelmed. There is, then, no concrete state to immunity, it being to quite an extent a variable of natural and human activities.

Notwithstanding the above observations, three separate levels of immunity can usefully be acknowledged. These are considered in increasing order of value to the individual.

1. short-term immunity
When a disease organism is detected, the body responds with a huge increase in the production of white blood cells, or leucocytes, which attack the invading organism. If the counter-attack is successful in containing and destroying the pathogen, and the patient recovers, then the body’s defences are demobilised and, after a few months, the leucocyte count returns to its original level.

The relevance of this type of defence is that the high level of overall resistance which quickly builds up within the human community during an epidemic of an infectious disease is an important factor in bringing about the collapse of the epidemic.

2. long-term immunity
Even when short-term immunity has been lost, the body’s defence system retains a ‘memory’ of the disease organism so that, should it return, the process of counter-attack can begin sooner and with greater strength. In the case of a viral attack, the resulting memory is usually lifelong whereas, after a bacterial attack, the body’s memory tends to diminish over some years.

3. natural immunity
An individual might possess the means by which to resist an invading pathogen as a result of an advantage genetically conferred from a previous generation. The advantage might be a relatively simple one, such as a certain blood type which hinders nourishment of the organism, or it may be more complex, involving a greater protective or enabling chemical constituency within the body’s defence system.

Natural immunity is an issue of prime importance when considering the temporal course of an infectious disease. In general, when a community experiences its first outbreak of a disease, deaths that occur will be among the susceptible, while members of the community endowed with a natural defence will survive. On a reappearance of the disease, more of the susceptible element will succumb, but the immune component of the community will again remain little affected.

After each outbreak, the susceptible-to-immune ratio alters in favour of the community which, in time, becomes made up almost entirely of members carrying a substantial degree of protection against the disease, one which can be passed on to future generations. The disease, although its pathogen may remain intrinsically unchanged, loses severity of effect, or disappears altogether from the human experience.

The temporal course of a disease, in which it becomes less virulent over time, may be interrupted or even temporarily reversed when large scale demographic migration takes place. During the process of urbanisation, for example, an urban community possessing a significant level of natural immunity as a result of repeated exposure may be joined by individuals from a rural environment perhaps having little or no previous contact with the pathogen. The migratory inflow will have the effect of weakening the overall immunity.

A further disturbance to the attenuating course of a disease can be the introduction into the community of the more virulent pathogen of another disease. The toll from the new disease may reduce the population threshold below that required by the original organism for successful dissemination, driving it into dormancy. Eventually, the virulency of the more recent organism will decline allowing the population density to recover and the earlier disease to resume its own temporal course.

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also known as
Charbon, splenic fever. The medical forms are: cutaneous anthrax, sometimes called malignant pustule; intestinal anthrax; and pulmonary anthrax, often referred to as wool-sorters’ disease.

causative micro-organism
Bacillus anthracis. Latin baculus, a stick. New Latin bacillus, rod-like. Greek anthrax, coal, lump of coal, carbuncle (boil).

type of micro-organism
Bacillus.

means of spread
Anthrax is primarily a disease of goats, sheep, and cattle. The bacillus rarely spreads directly from animal to animal but, when in contact with air, it forms extremely resistant spores which survive in suitable soils until being introduced to a new animal host during grazing. The disease enters the human domain from animals or animal products by the following routes:
1. by direct skin contact, to cause cutaneous anthrax;
2. by inhalation, to cause pulmonary anthrax;
3. by consumption of infected meat or milk, to cause intestinal anthrax.

effects on the human body
cutaneous anthrax
Incubation takes one to three days which is followed by an acute skin infection with lesions. Near a lesion the skin assumes a black appearance due to haemorrhaging below the surface. The lesions can heal, to leave scars. However, bacilli and debris from the infected areas may enter the bloodstream, resulting in blood poisoning and possibly death.

pulmonary anthrax
The entry of the bacillus into the lungs leads to pneumonia, with coughing and a spitting of infected blood, and to a certain death within one to four days of onset. This form of the disease allows transmission of the disease from human to human.

intestinal anthrax
Bacilli taken into the human alimentary system cause inflammation of the stomach with diarrhoea and vomiting. The illness can be severe but is not necessarily fatal.

Immunity patterns to anthrax are complex and are not fully confirmed.

historical profile
Anthrax was known in ancient times, and has always presented an occupational hazard to workers in agriculture, butchery, skinning, tanning, and bone crushing (for fertiliser).

Although the role of anthrax in human disease history has been comparatively minor, the pulmonary form approached epidemic proportions in the late eighteenth and in the nineteenth centuries as the factories of the Industrial Revolution began to process horse hair and sheep wool. In 1919 the Anthrax Prevention Act was introduced to prevent the importation of potentially contaminated material.

The bacillus of anthrax was described by Robert Koch in 1876 and, being one of the first disease organisms to be identified, became a cornerstone of his challenge to the miasmatic theory. In 1881 Louis Pasteur employed anthrax in trials held at Pouilly-le-Fort in France to demonstate the effectiveness of vaccination.

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also known as
Asiatic cholera.

causative micro-organism
Vibrio cholerae. Latin vibrio, I vibrate. Latin and Greek cholera, bile.

type of micro-organism
Vibrio. Because of its shape, the micro-organism of cholera is sometimes called a comma.

means of spread
By far the most common path of infection is by contaminated sewage coming into contact with water used for drinking, though the disease can also be transmitted through contact with the faeces of a victim. The vibrio can survive for some days on damp clothing.

Additionally, the housefly is known to act as a carrier; this means is of particular relevance where human ‘night soil’ is applied to the land as fertiliser. Transmission may also occur through domestic animals, which are not pathologically affected by the organism.

effects on the human body
The micro-organism enters the body by the mouth and, if it passes the acid barrier of the stomach, lodges in the small intestine, where it multiplies in enormous numbers. Typically, the process takes two to three days but in some cases onset can be within hours.

Vibrios produce a toxin which affects the permeability of various membranes. This causes a loss of fluid and essential minerals which is both very severe and rapid. Great quantities of ‘rice water’ diarrhoea are passed – possibly fifteen litres or more within a twenty-four hour period – containing millions of vibrios. The victim has no control over the motions. Vomiting also occurs. Clothes and bedding become highly contaminated.

Although there is no fever (body temperature actually drops), the patient, who takes on a characteristic ‘choleraic’ shrunken appearance, suffers muscular cramps and an extreme thirst. The blood thickens, blood pressure falls, and circulatory failure is possible. Death may follow.

If, however, a patient survives the attack then recovery is remarkably swift. There is normally no evidence of structural damage, though an attack of cholera does not offer any acquired immunity.

historical profile
The earliest reference to an outbreak of cholera possibly dates to a fourth century BC inscription in a temple near Gujarat, western India. Localised outbreaks in the sub-continent have been recorded throughout subsequent history. Recent research suggests that the vibrio resides in certain river plankton and can enter the human domain when the plankton seasonally bloom.

The nineteenth century witnessed a series of pandemics, which produced some profound social reactions. A first pandemic swept the eastern hemisphere from 1817 to 1823. This was followed by another which reached Europe, traversing the continental land mass from India, to reach England in October 1831. The disease continued to Ireland, from where immigrants transported it to North America. A further pandemic saw England’s greatest death toll from cholera, in 1848-1849. Again, the disease continued on to North America.

During an outbreak in 1854, Dr John Snow undertook his famous Broad Street pump demonstration in which cholera deaths in the London neighbourhood came to a sudden halt after he persuaded the authorities to stop water being drawn from a suspected source. Even so, the results of his experiment were largely ignored by the medical profession at the time. England was affected again by cholera in 1866-1867, and by minor outbreaks afterwards, though the disease continued on a greater scale elsewhere in Europe.

The vibrio was accurately described by Filippo Pacini in 1854 and isolated by Robert Koch and colleagues in 1883.

missed opportunity
An article headed ‘The cases of cholera successfully treated by large aqueous injections’ describing the basis for a perfectly adequate treatment for cholera appeared in the Lancet, 2 June 1832 (22, Vol II, 284-286).

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also known as
Croup (although this is also a general term applied to any obstruction of the upper air passages and characterised by a hoarse cough).

causative micro-organism
Corynebacterium diphtheriae. Greek koryne, a club; bakterion, diminutive of baktron, a stick; diphthera, a strip of leather or skin. There are three forms which are, in descending order of virulence, gravis, intermedius, and mitis.

type of micro-organism
Bacillus. The ends of the micro-organism are flattened out in a club-like manner.

means of spread
The disease is mainly transmitted from person to person directly by droplet infection. However, it can also be spread via clothes and bedding. Untreated milk may be an additional vehicle for diphtheria.

effects on the human body
The bacillus enters by the mouth and usually settles on the back of the throat, where it begins to multiply. In so doing, the micro-organism produces toxins which attack the membrane of the upper air passages. A ‘leathery’ deposit, sometimes called a false membrane, builds up on which the bacillus is able to multiply all the more. In the first week, the victim suffers a sore throat, a harsh cough, and a moderate fever. A characteristic ‘bull neck’ swelling develops. The disease is dangerous in two ways.

1. The false membrane composed of bacilli and dead cells, and the swollen tissues underneath it, begin to obstruct the passage of air, making breathing difficult. In severe cases, death from asphyxia (suffocation) can occur.

2. The powerful toxin of the bacillus enters the bloodstream to affect the nervous system, especially the sheaths of the peripheral nerves, and a paralysis may follow. But the most dangerous result of toxin in the blood, and the commonest cause of death from diphtheria, is heart failure.

Most deaths from diphtheria take place within the age group two to ten years. Complete recovery from even a severe attack is possible, though this may require some months. In some cases the bacillus takes even longer to be purged fully from the air passages and the individual thus becomes a carrier of the disease.

historical profile
The disease was reported in the eastern Mediterranean in the first centuries AD but does not seem to have become established in Europe until the eighteenth century. During the decade 1850-1860, a pandemic of diphtheria broke out, girdling the world by the end of the century. The bacillus was isolated in 1883 by Theodor Albrecht Edwin Klebs and was further studied by August Johannes Friedrich Loeffler, it being for many years known as the Klebs-Loeffler bacillus.

The late nineteenth century work on diphtheria is often seen as representing a turning point in modern medicine as regards effective prevention. Successful immunisation campaigns were instrumental in establishing pediatrics (the medical treatment of children) as a legitimate discipline. On the outbreak of the Second World War, immunisation against diphtheria was conducted on a national scale, and by the mid-1950s the disease had been virtually eliminated from the United Kingdom.

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specifically
Bacillary dysentery.

also known as
Campaign fever, flux, shigellosis. Greek dus, difficult; enteron, intestine.

causative micro-organism
Shigella. There are various species of shigellae, historically the most virulent being Shigella shigae, also called Shigella dysentariae. The micro-organism is named after Kiyoshi Shiga, who isolated shigae in 1898.

type of micro-organism
Bacillus.

means of spread
In an environment of poor hygiene and sanitary arrangements, especially in crowded conditions, bacilli from the faeces of an existing victim enter a new host on contaminated food. Following a non-fatal attack, bacilli can be passed in the motions for some time afterwards. The recovered individual therefore becomes a potential carrier of the disease during that period.

effects on the human body
Once in the human gut, incubation takes from a few hours to a week, the micro-organisms multiplying rapidly to cause an inflammation of the intestinal wall. Cases vary from mild to severe. In the latter, ulceration may occur. The almost continuous diarrhoea is accompanied by the passage of blood and mucus. Additionally to abdominal pains, there may be a fever, nausea, and vomiting. The most extreme ‘choleraic’ state of dysentery causes severe dehydration, and a shrunken appearance. Death may result.

historical profile
Dysentery has accompanied armies since ancient times, often proving to be more destructive than the enemy. The planned invasion of England by the French in 1779 was scuppered by the disease. Outbreaks affected the American Civil War, the Crimean War, and the First World War. On the domestic scene, the rise during the late nineteenth century in the use of cow’s milk, which when untreated provides an excellent growth medium for Shigella, caused heavy tolls among infants and young children.

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also known as
Flu, grip(pe).

causative micro-organism
Influenza Type A, B and C. There are many subtypes. Italian influenza, (cosmic) influence.

type of micro-organism
Virus.

means of spread
The highly infectious disease is usually transferred from person to person by airborne droplets, but can also be contracted from infected animals and through fomites.

effects on the human body
After inhalation, incubation takes two to three days. The virus attaches itself to the lining of the passages to the lungs, attacks the cells of the lining, and causes inflammation. A fever is often accompanied by a headache and pain in the limbs, with a general weakness which may persist. Although a patient might seem to recover, there can follow a long-term depression with possible repercussions later in life. In severe cases of influenza, the inflammation spreads into the lungs to cause pneumonia and possibly death.

historical profile
There is no convincing evidence of the disease prior to the Middle Ages, but several epidemics have occurred in recent centuries. The severe epidemic of 1557-1558, for example, killed Mary Tudor (‘Bloody Mary’) allowing her younger half-sister, Elizabeth, to ascend the throne. Three major pandemics swept Europe in the eighteenth century, with that of 1781-1782 perhaps being the greatest single manifestation of an infectious disease in history – over three-quarters of the entire English population is believed to have been affected. Epidemics also occurred in the middle of the nineteenth century and towards its end.

At the close of the First World War, a pandemic of Type A consisting of three waves swept across extensive areas of the entire globe. The source of the pandemic is said to have been traced to Fort Riley, Kansas, possibly entering the human domain from a pig, and the virus was transported across the Atlantic in troop ships. It appeared in England in the first week of November 1918.

Influenza dogged the Versailles peace conference of the following year. An estimated 500m people caught the disease worldwide; one official calculation put the global death toll at about 7m but mortality considerably in excess of this would be a more realistic assumption.

Type A reappeared in England in 1948. A subtype which came to be known as Asian Flu was responsible for a pandemic in 1957, and a further variation referred to as Hong Kong Flu broke out in 1968.

The chemical components that form the protein shell of the influenza virus undergo constant subtle rearrangement, a process called antigenic shift. Because the altered virus may not be recognised by the body during a subsequent attack, the prospects of acquiring a long-term general immunity to influenza are minimal. Consequently, the possibility of further pandemics of the disease in the future must remain likely.

the sweating sickness
During the Tudor period, five distinct waves of a mysterious, swift spreading, swift passing disease struck England and parts of Europe. Researchers in the earlier and middle decades of the twentieth century believed the enigmatic disease to have been caused by an unidentified strain of influenza, though the theory has more recently lost much of its previous support. nonetheless, the sweating sickness, or Sudor Anglicus as it was also known, still awaits a convincing alternative explanation.

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also known as
Hansen’s Disease. Named after Gerhard Henrick Armauer Hansen, who isolated the bacillus in 1873.

causative micro-organism
Mycobacterium leprae. Greek mukes, mushroom (employed in this sense to mean fungus-like); bakterion, diminutive of baktron, a stick; lepein, to peel.

type of micro-organism
Bacillus. The micro-organism is related to that of tuberculosis but has a predilection for human nerve coverings and skin.

means of spread
Leprosy has a low infectivity and is slow to develop, requiring close and continuous human contact in unhygienic conditions. The actual mechanism of transmission is not proven but the disease probably passes from person to person mainly by nasal secretions, the nasal cartilage being a common site for bacterial growth.

effects on the human body
There are two ‘poles’ to the disease, with every intermediate possibility, though incubation may take several years.

1. lepromatous leprosy
The skin becomes scaly and covered in lesions called leproma. The leproma can ulcerate, discharging micro-organisms. A steady destruction of tissue takes place.

2. tuberculoid leprosy
The sheaths of the nerves in the limbs are affected, below the knees and elbows, in the cooler parts of the body. Sensation is lost, muscle wastes away, bone decalcifies. Severe deformity results. The insensitised areas are prone to accidental physical damage and secondary infection, which may in severe cases lead to death.

In any form of leprosy the eyes are frequently affected, with a loss of movement and blink reflex. There is a painful inflammation. Blindness may follow. Involvement with the vocal cords can produce a characteristic raspy voice.

historical profile
Although leprosy is an ancient disease, it did not become prevalent in Europe until the sixth and seventh centuries. It began to recede in England in the thirteenth century but persisted in continental Europe for a further two centuries and in Scandinavia until the nineteenth century.

A definitive explanation for the decline of leprosy has yet to be found, though one theory contends that the related and swifter acting tuberculosis bacillus took over, while another examines the part played by the increased intake of vitamin C. This is believed to repress the chemical process whereby the bacillus of leprosy feeds on human tissue.)

Perhaps because of the traditions of the Bible, reproduced by religion, the fear of infection from the disease was exaggerated during the Middle Ages. Lepers not only suffered the ravages of the micro-organism but were also excluded from mainstream society.

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also known as
Ague, blackwater fever, padulism. Italian mal aria, bad air.

causative micro-organism
Plasmodium. The main species are Plasmodium falciparum (the most virulent), Plasmodium vivax, Plasmodium ovale, and Plasmodium malariae. Greek plasma, moulded; desmos, bond.

type of micro-organism
Protozoon.

means of spread
The organism enters the human domain through the feeding bite of the female anopheline mosquito (Greek anopheles, hurtful), of which there are about thirty species able to transmit the protozoon. The female takes blood meals in order to obtain protein for egg production whereas the male, feeding on nectar, is not involved in the transmission of malaria.

In addition to the mosquito, an infected human can introduce the disease to a hitherto unaffected area. A mosquito may feed from the victim and thus pass the protozoon to other humans, who in turn infect further mosquitoes, and so on. The preferred breeding grounds of the mosquito are marshes and swamplands.

effects on the human body
Although the protozoon is a simple animal form, its life cycle is complex. The essential pattern is as follows. When the mosquito takes a feed, its saliva introduces the disease organism into the human body. At this stage, the protozoon is in its sporozoite form (Greek sporos, seed; zoe, life). Once in the human bloodstream, the sporozoites collect in the liver, where they invade the cells and multiply as merozoites (Greek meros, part), a process that may take one or two weeks.

The merozoites are in turn released into the circulatory system, where they utilise the red blood cells either to multiply further, or to produce gametocytes, which are sexed (Greek gamos, marriage, reproductive union; kutos, vessel). Gametocytes are carried around in the host’s blood until an uninfected mosquito takes a feed. In the mosquito’s digestive system, the sexed gametocytes mate to form a zygote (Greek zygon, pairing) which enters the wall of the insect’s stomach from where sporozoites are produced. And thus another cycle is ready to begin.

Merozoites are released from the liver more or less in batches. The body responds with a fever. After a shaking chill, a drenching sweat breaks out. Nausea, vomiting, and a severe headache accompany the reaction. Certain organs are damaged as the red blood cells fall to the merozoites. The destruction of red blood cells causes the urine to turn dark red or black, hence the term blackwater fever sometimes being applied to malaria. In some cases the brain is affected when delirium, coma, and death may ensue.

The various species of Plasmodium produce different rhythms of merozoite release. For instance, the merozoites of falciparum are released every twenty-four hours, those of vivax and ovale every forty-eight hours, and the merozoites of malariae every seventy-two hours. Death from falciparium is more likely than from the other species, although the human individual may receive dangerously high levels of any of the malarial species if bitten by enough mosquitoes. There is also the probability that some sporozoites may lie dormant in liver cells for months or even years, to reappear suddenly as merozoites.

No full personal immunity to malaria is acquired, though repeated attacks by the same species tend to reduce the effects. Artificial immunisation against the disease is not possible; instead, chemical agents are administered.

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historical profile
Malaria protozoa can be traced back to before the evolution of mankind. The ancient Egyptians made references to the disease; Hippocrates detailed it; and the Romans were able to make use of it as a defence measure, the Campagna Romana marshes around their capital providing a debilitating barrier to would-be invaders. Malaria, especially of the Plasmodium vivax species, was once fairly common to temperate countries such as England, where the marshes of East Anglia provided breeding grounds for mosquitoes until the eighteenth century.

In 1658, Oliver Cromwell, Lord Protector of the Commonwealth following the English Civil War, and born in the Fenlands, succumbed to an attack of malaria. The disease was almost certainly introduced to the New World during post-Columbian contact, the protozoon taking readily to the central American regions.

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also known as
Morbilli, rubeola.

causative micro-organism
Morbillivirus. Latin morbilli, little disease (to distinguish it from plague, the ‘big’ disease).

type of micro-organism
Virus.

means of spread
This disease, the most infectious of common fevers, is transmitted primarily by droplet infection but it is also spread by direct contact and via clothes and bedding. Human beings represent the only reservoir of the measles virus.

effects on the human body
Within ten days of the virus entering the body a fever begins. Shortly before the fever, distinct ulcers appear in the mouth. These are known as Koplik’s spots (after Henry Koplik, who formally associated them with the disease in 1896, although their significance was known earlier). About four days after the outbreak of fever, a rash of blotchy red spots appears on the skin. The usual pattern of spread of the rash is head to body to limbs.

Because of a widespread inflammation of the respiratory tract, a measles victim is prone to secondary bacterial infection which may lead to complications, such as pneumonia, that could prove fatal. An attack of measles also gives cause for concern during early pregnancy. Otherwise, the rash fades and the disease leaves the body, conferring a life-long immunity. Since most adults are already immune, the disease generally attacks only children, who themselves then carry immunity into adulthood.

historical profile
The origins of the virus are unknown since, historically, the disease was confused with smallpox. Persian physician al-Razi (Rhazes) distinguished the two in a treatise of AD 910, but the confusion continued in Europe until the early modern period. In the numerous epidemics of the seventeenth, eighteenth and nineteenth centuries, it is thought that virtually no European child escaped exposure to the virus and this is why the disease has such a relatively mild effect today.

However, the virus is able to inflict high mortalities on previously unexposed populations, as was the case when Europeans introduced it into the Americas and the Pacific islands. The last outbreak with serious consequences occurred in Greenland in 1951.

German measles
Generally milder than measles, an infection of German measles, or rubella, is caused by a different virus. There is a similar type of rash but incubation is longer (about three weeks) and there are no Koplik’s spots. The main risk from German measles is to the foetus, especially during early pregnancy, when congenital rubella syndrome (CRS) is likely to occur, causing abnormalities such as cataracts, deafness, damage to the central nervous system, mental retardation, and physical defects. An abortion is often advised.

The history of rubella is confused with those of other diseases, notably measles and smallpox. Its common name probably arose because early work on the disease was dominated by German physicians, particularly Daniel Sonnert, though another opinion links the term with the word ‘germane’, in the sense of being closely akin to (measles). The name rubella was suggested by Henry Veale in 1866.

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also known as
Bubonic plague. Greek boubon, groin. Latin plaga, a blow, a stroke.

causative micro-organism
Yersinia pestis. Named, following a reorganisation of nomenclature in 1971, after Alexandre Emile-Jean Yersin, the first investigator positively to identify the organism, during the Hong Hong outbreak of 1894. Previously, the bacillus was known as Pasteurella pestis.

type of micro-organism
Bacillus.

means of spread
There are two distinct ways in which the bacillus spreads throughout a human community, and both normally occur concurrently.

1. bubonic plague
The disease begins its epidemic course in this form. Plague is essentially a disease of rodents, in particular Rattus rattus, the black rat. The bacillus is transmitted into the human domain chiefly by the black rat’s principal flea Xenopsylla cheopis. Bubonic plague is therefore a contagious disease, requiring a vector. In general, without a flea bubonic plague cannot spread.

2. pneumonic plague
Victims having the bacillus in their lungs will cough out infected droplets, which can be inhaled by anyone in close proximity. Pneumonic plague is thus a truly infectious disease, transmissible with no direct contact necessary.

effects on the human body
When the flea takes a blood feed from an infected rat, the flea itself often becomes infected. The rat normally dies from plague and the flea seeks another host, so passing on the disease. As rat numbers dwindle, the flea has little choice but to accept an alternative mammalian host – such as man.

The human body’s response on being injected with plague bacilli by the flea is to filter out the micro-organisms at the nearest lymph node for destruction and disposal. Since the leg is the most frequent site of flea feeding, the lymph node in the groin is thus the most likely to be affected. Hence the name bubonic plague (Greek boubon, groin).

However, within the lymph node the bacilli multiply more rapidly than the body’s defence system can overcome them. The intensely painful node ruptures, usually internally. Bacilli enter the blood stream. A feature of Yersinia pestis is that it not only produces toxins when active, but if killed, other toxins are released from its casing. Dead or alive, the micro-organism of plague poisons the blood.

Toxins spread throughout the body, killing the body’s cells. Blood vessels are eaten away, allowing blood to ooze into tissue space. Near the body’s surface this process gives rise to characteristic areas of blackened skin. The victim experiences headache, vomiting, giddiness, thirst, pain in the limbs, intolerance to light, sleeplessness, and possibly delirium. The heart pounds faster as blood pressure drops. If the body cannot stop the bacilli then death from shock occurs. The bubonic course generally takes but a week.

In some cases the bacilli enter the lungs from the bloodstream. There they multiply, giving rise to the highly infectious pneumonic plague. Pneumonic plague is invariably fatal to the victim, and to anyone else who inhales the infected droplets coughed out by the victim, death occurring in one to three days.

It is sometimes believed that there is a third form of the disease called septicaemic plague. In fact, this can be taken to represent the final stages of plague, when bacilli teem in vast numbers throughout the body, and death is assured. On occasions, the bubonic stage is bypassed because bacilli enter the bloodstream directly. The first stage is in effect the final stage, and the victim dies within hours. An important aspect of septicaemic plague is that, because the blood is so loaded with bacilli, the human flea, Pulex irritans, is able to transmit the disease to another host once the original host dies.

historical profile
Old Testament references to plague among the Philistines in the eleventh century BC are controversial but, although a certain caution is required, they are not necessarily incorrect. Another outbreak may have occurred in Egypt around 300BC. But the confirmed history of plague is split into three pandemics. For plague, the term ‘pandemic’ often assumes a modified reference, not to a single event but to a series of cycles.

first pandemic
The disease, possibly originating in East Africa, arrived in Constantinople, capital of the Byzantine Empire, in 541. The death toll of this epidemic, sometimes called the Plague of Justinian after the emperor of the time, was considerable. Plague spread around the Mediterranean, causing a substantial depopulation. A further sixteen cycles have been identified, the sequence ending about 760.

Wolfenstein the new order keygen serial key generator. second pandemic
The initial wave is known as the Black Death. Originating in one of divisions of the Mongol Empire, possibly because of climatic changes, the disease cut a massive circular swathe of death through Europe, finishing close to where it began. At the same time, a separate arm devastated the Islamic Middle East. China was also severely affected.

Plague entered England in 1348, causing most of the estimated 1.5m deaths in 1349. From 1361 to 1665, thirty-three cycles of plague are traceable on a national scale. Eastern Europe, often dominated by the numerous phases of the Russo-Turkish War, continued to experience plague to the end of the eighteenth century.

third pandemic
Beginning in south-west China in 1873, the disease reached Canton in 1894 to kill more people than did the Great Plague of London in 1665. A similar toll resulted in Hong Kong. It was here that the bacillus was first identified. From Hong Kong, the disease was transported to India, where an estimated 12.5m people died of plague between 1897 and 1957. The bacillus spread to Australia, North America, South America, and South Africa.

Partly because of the intervention of modern medicine and preventative measures, the Third Pandemic has had little opportunity to exhibit plague’s cyclic nature, though minor outbreaks and cases of the disease continue to be reported in various parts of the world.

Yersinia pestis has probably shaped history more than any other micro-organism. No other disease has been able to influence population trends for such long periods. Each pandemic involved a different strain of the bacillus (in turn, antiqua, mediaevalis, and orientalis). Although numerous local theories have been tendered to explain the passing of the Second Pandemic from Europe, it can be argued from a more global standpoint that both this and the First Pandemic were essentially brought to an end by a build up of natural immunity.

Plague in England: national epidemics 1348-1665
effect on England’s population
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also known as
Scarlatina.

causative micro-organism
Streptococcus pyogenes. Greek streptos, twisted; kokkus, berry; pyon, pus; genes, born, be produced.

type of micro-organism
Streptococcus (Group A). The streptococci represent a large group of bacteria which were first identified by Christian Albert Theodor Billroth in 1874 and classified into an alphabetical sequence by the American bacteriologist Rebecca Craighill Lancefield in 1933. Group A streptococci are called pyogenes. The name means pus-forming and relates to the debris of dead organisms and cells which results from the battle between bacteria and antibodies.

means of spread
Streptococci are normally spread from person to person by airborne droplet, especially in overcrowded or poorly ventilated conditions, but may also be transmitted in untreated milk and on food. Moreover, streptococci can also reside in an individual who is not affected by them and is thus a carrier.

effects on the human body
A wide range of infections may result from the entry of Group A streptococci into the body. When access is by inhalation, the organisms colonise the upper air passages to initiate, for example, tonsillitis. Some, however, produce a particular toxin which spreads round the blood system, causing damage to the capillaries. This course manifests itself by a rash of tiny red spots on the skin and the characteristic ‘strawberry tongue’ of scarlet fever. Within twenty-four hours of contracting the disease, the victim suffers a sore throat, headache, vomiting, and a fever. In severe cases, the toxin causes circulatory failure and death.

One possible consequence of an attack of scarlet fever is an abnormally high production of antibodies and, about two to three weeks after the primary illness, a reaction results in an attack of acute rheumatic fever. This development tends to recur over a period of years leading to organ failure, especially of the heart. Rheumatic fever is also associated with Sydenham’s chorea (named after Thomas Sydenham), known more commonly as St Vitus’ dance.

historical profile
Scarlet fever seems to have waxed and waned over the centuries but was severe both at the beginning and towards the end of the nineteenth century, being at one time the main cause of childhood deaths, with children in the age group two to ten particularly susceptible.

puerperal fever
Another infectious disease of some historical consequence brought about by Streptococcus pyogenes is puerperal fever, once known as childbed fever. The organism invades the birth canal and adjacent tissue during childbirth and the symptoms – lethargy, poor appetite, fever – usually appear within five days, although much longer incubation periods have been noted.

There can be little doubt that medical practitioners and nurses were at one time significant disseminators of the disease; in fact, both Oliver Wendell Holmes and Ignaz Semmelweis independently found, during the 1840s, that infection could be substantially reduced merely by applying basic measures of hygiene during childbirth.

staphylococcal infections
Related to the streptococci are the staphylocci (Greek staphule, a bunch of grapes; kokkus, berry). The principal form is Staphyloccus aureus (Latin aureus, golden), so named because of its pigmentation. Staphylococci often enter the body through breaches in the skin and via the ducts of the sweat glands. Their toxins cause local inflammation and, carried by the blood, possibly more serious remote complications. Thus, boils, carbuncles and abscesses are the normal products of a staphylococcal infection, but the alimentary and respiratory systems may be affected, with the possibility of pneumonia.

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also known as
The pox, becoming known as smallpox in the sixteenth century to distinguish it from syphilis (the great pox).

causative micro-organism
Mainly Variola major, although there are other variola types. Latin varius, changing, diverse.

type of micro-organism
Virus.

means of spread
Smallpox is transmitted from person to person by inhalation, and from the sores of a victim. Clothing and bedding may act as fomites.

effects on the human body
Within a week of contracting the virus, the individual will suffer a severe headache, fever, backache, and perhaps vomiting, convulsions and delirium. Children are especially prone to the latter effects. Open sores appear in the lining of the throat, from which the virus is able to spread around the body in the blood system, reaching the liver and spleen. In these organs it replicates rapidly to re-invade the blood system.

After a further three or four days a rash of small, flat reddish spots appear on the face, followed by the limbs and trunk. (The virus actually attacks and destroys the sebaceous glands; these produce sebum, or skin oil, and are more numerous on the face.) Over the following couple of days, the spots turn into blisters, or pustules, filling with a clear fluid. Sometimes the blisters can be hideous, resembling the effects of a burn or scald. Towards the end of a week, the fluid in the blisters turns yellowish and pus-like, giving off an unpleasant odour.

Eventually the blisters dry up, leaving a crust or scab on the skin. When the scab falls off, at some time during the next month, a pit is left behind in the skin – especially so after facial blistering. Throughout the entire course of the attack, the disease is extremely infectious. Millions of viruses are present, first in the throat sores, then in the pustular fluid.

Additionally to the skin, the virus attacks the lungs, heart, and other organs, causing haemorrhaging and blood poisoning. Death can occur. Survivors are usually pock-marked but are completely immune to further attack. However, ulcerations on the cornea can possibly lead to permanent blindness, and damage to the sperm duct may result in male sterility.

historical profile
Variola major may have evolved from forms that still persist in animals during the period when those animals were undergoing domestication. The process would have been greatly facilitated by animals and humans sharing the same roof. There is clear evidence of smallpox in Egyptian mummies dating from 1570BC.

The virus entered Europe at an early period, and most certainly appeared in England before the Crusades, though its continental spread had to await a certain density of population, which did not arise until the thirteenth century.

Subsequent depopulation caused by plague seem to have kept smallpox in check, but as populations began to recover in the sixteenth century, the intensity and frequency of smallpox epidemics increased. Elizabeth I contracted the disease in 1562 but survived. Not so Mary II; and the death of the 11-year-old Duke of Gloucester – one of Anne’s seventeen children, none of whom reached adulthood – from smallpox in 1700 effectively meant the end of the Stuart dynasty.

The introduction of smallpox to the New World in the sixteenth century had a devastating effect on the central American civilisations. It also continued to be one of the main epidemic killers of seventeenth century England.

Practical medical attempts to counter the disease began early, with a description of inoculation being published in 1714 and the measure being widely practised by mid-century. Edward Jenner introduced a new term to the language when he ‘vaccinated’ (Latin vacca, cow) a boy in 1796 with matter taken from a cowpox lesion on a milkmaid’s hand. Jenner’s technique, in which he introduced a weaker viral type into the human body, was much less risky than the hitherto inoculations of Variola major.

Partly as a result of the practice, smallpox cases declined steeply in the early nineteenth century. In 1939 England was declared completely rid of the disease, and in 1979 the World Health Organisation announced world freedom from smallpox.

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also known as
The great pox, to distinguish the disease from smallpox. Later, syphilis was sometimes known simply as the pox. Other references at various times have been (in England) the French Pox, Lues venerea, Morbus gallicus, and venereal syphilis. The disease took its name from Syphilis, sive Morbus Gallicus, (Syphilis, or the Gallic Disease) a poem written in 1530 by Girolamo Fracastoro, in which the main character, an erring shepherd called Syphilus, became infected as a divine punishment.

causative micro-organism
Treponema pallidum. Other treponemes are responsible for enteric syphilis, pinta, and yaws. Greek trepein, to turn; nema, a thread. Latin pallidus, pale.

type of micro-organism
Spirochaete.

means of spread
The spirochaete is transmitted from an infected person to a new host usually through sexual intercourse, although it can also enter the body via a skin abrasion on close contact with an infected person.

effects on the human body
Syphilis is a disease of the blood vessels. Its action is divided into two chronologies, with three stages recognisable in all.

primary phase (early syphilis)
The spirochaete penetrates mucous membrane to enter and spread throughout the blood system. Near the point of origin a sore, or chancre, appears, usually after three weeks or so. If transmission was through sexual intercourse, for the male the chancre appears on or near the head of the penis, for the female on the labia or within the vagina. The chancre, which persists for about a month, teems with spirochaetes.

secondary phase (early syphilis)
At some time in the following half year, though usually earlier rather than later, a general rash will appear as the spirochaetes disperse throughout the body. This is accompanied by thin sores in the throat and mouth, on the genitalia, and within the rectum. There may be a headache and fever, and the joints could become painful, especially at night. Syphilis remains highly transmissible during this phase, which may last two years.

tertiary phase (late syphilis)
This phase could occur soon after the secondary phase or quite some years later. Although the disease is less infectious, it presents extreme danger to the victim. The spirochaete is able to invade any cell of the body, causing damage to organ or structure. For instance, it may attack the central nervous system to cause loss of positional sense; the brain to bring a distinct form of insanity termed general paralysis of the insane (GPI); the eye, to cause blindness; or the heart, resulting in the failure of that organ.

The disease can be genetically passed down in a form known as congenital syphilis. Defects to sight, hearing and bone structure may occur in offspring in a pattern known as Hutchinson’s Triad (after the formal description by Jonathan Hutchinson in 1861). The liver and kidney could also be affected. In some cases, congenital syphilis may not manifest itself until puberty.

historical profile
Two principal theories exist to explain the origins of syphilis. For a long time the Columbian theory has held sway. This holds that syphilis was introduced to Europe by the crews of the late fifteenth century ‘discoverers’ of America, who had sexual intercourse with native women.

The other, the Unitarian theory, prefers to believe that all treponemes originated from one African source, Treponema pallidum adapting to venereal transmission because its potential hosts in the temperate regions of Europe wore more clothes. Promoters of the Unitarian theory point to various references in Deuteronomy and other Old Testament sources.

The fact remains, however, that the earliest reliable description of syphilis in Europe dates after the Columbian discovery of America, and within five years of the return of the venturers the disease had spread throughout Europe, each nation tending to name the disease derogatorily after its neighbour. It continued its course to the Middle East, then to the Far East, the symptoms apparently being described in a Japanese writing of 1512.

Ironically, syphilis was not recognised as a sexually transmitted disease until the seventeenth century. The pale, slender causative micro-organism was discovered in 1905 by Fritz Schaudinn and Erich Hoffman, who gave it the earlier name of Spirochaeta pallida.

A year or so later August Paul von Wasserman developed a test (now superseded) which was able to show the presence of the disease in any of its stages. In the twentieth century a resurgence of syphilis occurred amongst troops of all nations during the First World War and to some extent during the Second World War.

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also known as
Consumption, phthisis, the white plague.

causative micro-organism
Mycobacterium tuberculosis. Greek mukes, mushroom (employed in this sense to mean fungus-like); bakterion, diminutive of baktron, a stick. Latin tuberculum, diminutive of tuber, node, swelling. Greek -osis, abnormal condition.

type of micro-organism
Bacillus. TB, the common abbreviation for tuberculosis, stands for tubercle bacillus.

means of spread
The principal entry into the body is by inhalation, though the disease can be contracted from milk and other dairy products taken from infected cattle. In rare cases it can also be transmitted via infected urine. Frequent exposure to victims substantially increases the risk of infection. If not revealed to sunlight, the bacillus can survive for months in dried sputum, and is able to multiply in damp, dark environments.

effects on the human body
There are two stages to the disease.

primary infection
This initial stage usually occurs in childhood. The bacillus reaches the middle and lower lung areas to gain access to the bloodstream. It subsequently lodges in any organ. Childhood symptoms are often lethargy, poor appetite, loss of weight, and fever. Although the disease is normally contained, the body does not rid itself of the bacillus – instead the disease is said to become quiescent, or dormant. No immunity is developed.

In certain cases, the bacillus enters the bone structure, especially that of the spinal column, to produce later deformities such as a hunched back or ‘spidery’ legs. This course is known as Pott’s Disease. Male children are more prone to Pott’s Disease than are female.

secondary infection
If the individual is re-infected or if the body defences are lowered through malnurishment, injury, attack from another disease, or – in females – as a result of childbirth, tuberculosis can enter its secondary, or chronic, stage. This may emerge several decades after the primary infection and usually takes place in a particular part of the body.

By far the most common form of the disease is pulmonary tuberculosis. The first symptoms can be slight: a listlessness and a vague pain in the chest; but the situation worsens to cause a sharper pain, shallow breathing, chills, fever, and an acute and exhausting cough accompanied by a spitting of blood.

A frequent consequence of pulmonary tuberculosis is inflammation of the airtight membrane that surrounds the lungs. The cavity that contain the lungs is maintained in a healthy individual at less than atmospheric pressure in order for the lung to operate correctly. In a tuberculosed person the airtight membrane can eventually be perforated by the bacillus, causing a sudden collapse of the lung.

Another possibility is the development of broncho-pneumonic tuberculosis, wherein the linings of the bronchial tubes are rapidly destroyed. This usually fatal course was at one time known as ‘galloping consumption’.

With tuberculosis, it is not the bacillus itself that causes the harm – for instance, it does not release any toxic material. Instead, the body responds to the micro-organisms in the normal way by killing them, but rather than the debris being cleared from the site it steadily builds up a deposit to form ‘cheesy’ (or caseous) tubercles. It is the tubercles that cause the inflammation and destruction.

Moreover, wherever the bacillus might be lodged in the body, its requirements cause a vitamin deficiency in the human host. The situation can be exacerbated by a loss of appetite for food. In short, the body is not able to repair itself adequately and becomes ‘consumptive’.

historical profile
There is evidence that prehistoric communities suffered from tuberculosis. In more recent times, the suggestion is that, on the retreat of plague, tuberculosis became the major killer disease in Britain. It often went undiagnosed and under-reported as such until the nineteenth century, but the bacillus would seem to have been extremely widespread throughout society.

Among the lower classes, poor domestic and working environmental conditions were unquestionably responsible both for a primary infection during childhood and a secondary infection in adulthood. Despite traditional opinions, recent studies are unable to confirm climate as a direct factor in the spread of tuberculosis.

The causative micro-organism was discovered by Robert Koch in 1882 but he misunderstood the disease, his subsequent search for an effective tuberculin (an extract of the bacillus with which to provide immunisation) causing much controversy. In 1906, Léon Charles Albert Calmette and Camille Guérin began work on a vaccine from a weakened strain of the bacillus which, after many years work, culminated in the preparation of BCG – Bacille (or Bacillus) Calmette-Guérin.

Although it does not give complete protection, BCG helps the body to counter tuberculosis and has been widely used since the Second World War. After a generation of vaccination it was considered that the battle against tuberculosis might be all but won, but since the late 1980s the number of cases among the industrialised nations – including the United Kingdom – has begun to rise.

scrofula
Known historically as the King’s Evil, but also known medically as scrofuloderma, the details of scrofula’s precise clinical development are far from simple. A plausible cause of what is essentially tuberculosis of the skin is through an infection contracted while crawling as an infant in the presence of an adult suffering pulmonary tuberculosis who habitually spat onto the floor. The face can be affected, and in severe cases hideous deformities may develop.

In earlier centuries, scrofula was apparently widespread, but it was contemporaneously believed that the king possessed the power to heal it. The ceremony of the King’s Touch began for sure in the eleventh century in France and was adopted by Henry II in England during the twelfth century, although Edward the Confessor may have practised similar rites. With some exceptions, the ceremony was carried out by English monarchs until the Hanovers refused to continue it, the last occasion possibly being 27 April 1714 conducted by Queen Anne shortly before her death.

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also known as
Enteric fever.

causative micro-organism
Salmonella typhi, named after Daniel E Salmon, an American pathologist. The disease was formally distinguished from typhus in 1829. Its causative micro-organism was identified by Carl Josef Eberth and Theodor Albrecht Edwin Klebs in 1890.

type of micro-organism
Bacillus.

means of spread
The bacillus is contracted from contaminated food and drinking water, and from infected shellfish taken from sewage-contaminated sea and river waters. The disease is also spread by flies which come into contact with human faeces, a frequent source of infection when ‘night soil’ was applied to the land as a fertiliser.

effects on the human body
The micro-organism enters the body through the mouth and, if it survives the acid barrier of the stomach, passes to the small intestine, where it multiples. Some of the symptoms are similar to those of typhus: after a week or so, the victim suffers a headache, a sore throat, and loss of appetite. The bacillus then invades the blood stream to reach the liver and spleen, where further multiplication takes place.

There follows a fever, lasting perhaps for two weeks, and red spots appear on the chest or abdomen. Diarrhoea is often present and, in severe cases, a delirium takes hold. Intestinal haemorrhaging and perforation of the bowel may occur, with death likely.

Where recovery takes place, the bacillus often lodges in the gall bladder. The patient gains an immunity to further attack but may become a carrier, a number of micro-organisms passing out of the body during each defecation.

historical profile
Typhoid fever is considered to have once been widespread though, because of its relatively late recognition as a disease distinct from typhus, it has perhaps been misrecorded in the historical record. Nevertheless, typhoid produced one of the best documented examples of a human disease carrier.

Mary Mallon, an Irish cook, emigrated to the United States at the end of the nineteenth century. Because typhoid fever invariably appeared in the households and establishments which employed her, she became known as Typhoid Mary. No solution could be found other than to isolate her from society, and she was legally detained for twenty-three years until her death in 1938.

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also known as
Camp fever, famine fever, gaol fever, jail fever, ship fever, war fever, spotted fever, or el tabarillo (Spanish, red cloak). Medically known as louse-borne, or classic typhus, to distinguish it from other strains of typhus spread by alternative vectors. Greek tyfos, fog, haze, smoke, stupor.

causative micro-organism
Rickettsia prowazekii. Named after Drs Howard Taylor Ricketts and Stanislaus Josef Mathias von Prowazeki, both of whom died from the disease while investigating it.

type of micro-organism
Rickettsia.

means of spread
Typhus is disseminated through a community by the human body louse, Pediculus humanus corporis (or vestimentia) and sometimes by the head louse, Pediculus humanus capitis. The principal precondition for a typhus epidemic is overcrowding in a situation of squalor or undernourishment, especially where the same clothes are worn for lengthy periods. In such circumstances the spread of typhus is extremely rapid.

effects on the human body
The micro-organism multiplies in the intestines of the louse to the extent that if the louse does not defecate frequently then it will die. Under such circumstances, the louse will assuredly defecate as it feeds. When the louse takes nourishment from the human host the skin site is irritated and the victim massages the area in order to relieve the itching sensation, thus rubbing the louse’s infected faeces into the puncture caused by the feeding.

Incubation of the disease takes one to two weeks during which the victim suffers headache, a running nose, a cough, nausea and chest pain. This is followed by chills and a high fever, vomiting, constipation, muscular aches and perhaps delirium. A rash of red spots covers the trunk, arms and legs. Either the victim dies or the disease passes after a couple of weeks, leaving an extreme weakness. The lice seek new hosts during the fever stage, when the victim’s body temperature becomes uncomfortably high, thus ensuring a rapid spread of the disease in conducive conditions.

The disease can re-emerge in the individual when defences are low, even after some years. When this occurs, it is usually known as Brill-Zinsser Disease (after Nathan Edwin Brill and Hans Zinsser).

historical profile
The early history of typhus remains something of a mystery but the micro-organism seems to have been introduced to Europe from the Middle East in the fifteenth century. As the nineteenth century opened, the disease experienced a dramatic increase of prevalence. Napoleon’s attempted invasion of Russia, 1812, was severely hampered by typhus.

Ireland suffered a widespread epidemic during the period of famine 1816-1819, and another after the failure of the potato crop in 1846. Irish emigrees, escaping the famine, transported the rickettsia to America. In the twentieth century, typhus epidemics occurred among the inmates of German concentration camps.

relapsing fever
Although similar in many ways to typhus, relapsing fever is caused by a spirochaete, Borrelia recurrentis. It affects th liver, making the victim jaundiced. The fever may reappear a few days later, the cycles perhaps repeating three or four times. Mortality can be high, and immunity is short-lived.

The history of relapsing fever is unclear since it was not separated from that of typhus until 1843, but as both rely on the human louse for transmission there is no reason why both should not sometimes occur concurrently.

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Original document prepared by Brian Williams BA (Hons) in 1997 for distribution within the Department of Economic and Social History at the University of Hull, England.

Are Croupbeatz.com Drums Bangin?

If you’ve been around sounds and sample libraries for a while you know that a lot of times things tend to be more the same than different.

However…

If you’ve been around any hip hop or underground music forums then you’ve no doubt heard about Croup! Croup is a producer of that classic, “golden era” sound of course with his own style.

But we aint talkin bout croup the producer, we talking bout croup the sound designer!

Yes, I’m sure many of you have heard of the legendary “Deadly Drums” from Croup. Not to be confused, croup is the originator of deadly drums, there is ONLY ONE. He has been selling his drum kit via forums and myspace for quite a while.

Anytime they are mentioned, they are stated as being “must-haves” for any producer.

You know I had to find out for myself, because I too have ran into a post or two about croup and his drums.

And I must confess, I got my hands on a demo of his kit years ago and they remain in my toolbox…well, until he sent over the full collection for review. So let’s see whatsup with them.

Croupbeatz.com Deadly Drums

Dirty, hard, ruff, rugged, nasty, crunchy, BANGIN! Just a few words that come to mind when you crack open this treasure chest of head noddin potion.

I didn’t know what to expect when opening this package, but I was pleasantly surprised.

Not only were there drum sounds, but Croup included instrument snippits and riffs, bass, and even sfx to help you fill out your tracks.

Not only do you get the ingredients for the foundation of your track, but you can make a complete tracks with the sounds in this kit.

Most importantly, the drum are HARD. Nothing pisses me off more than to read the discription of a drum kit, claiming to be hard, bangin, or whatever…only to get a collection of impotent drum sounds. Check the video to see what I mean. Croup brings the ruckus on this one.

Croupbeatz.com Filthy Drums

A little while later, after everyone praised him for deadly drums, croup followed up with part 2.

Filthy drums picks up where deadly drums left off, croup decided to focus mainly on drums for this volume.

Realizing people usually have their own sounds and samples, but that being the fanatical beat fiends that we are, we are CONSTANTLY looking for fresh, bangin, drum sounds.

Some will remain purists, and chose to chop and mold their own drums…more power to ya! I do that too, but I don’t sleep on the fact that other people have records, gear, or even a different ear than I do.

All that comes in to play. And when you want a stash of high calibur sounds at your disposal, you MUST build up a solid drum library.

Filthy drums comes with that same deep, crunchy, dirty, sexy, head bangin feel you want from your drums. Not for the raido friendly bubble gum pop tunes (not that there’s anything wrong with those) These are those of you that like to walk on the dirtier side of the track. Peep the video.

So What’s The Verdict?

Basically, if you produce any type of rugged, drum heavy, boom bap, underground, dirt on ya fingers, gutter, non bubble gum music then this is the kit to have.

Forget the bull, forget the “purity” of diggin for drums, please add these to your collection. Yes, you can still eq and layer and all the good stuff….but…if you start wit trash…you can’t cover trash up.

Any true drum fanatic will fall in love immediately.

The sounds have punch, they are clear, not distorted, but definitely bangin!

I’ve tried many drum sounds, from commercial to free libraries, and I too chop up and create my own drums.

But I’ve got to say, the drums in this kit are amazing.

Now, I don’t think you’ll use every single sound…I only need a few dope kicks and snares to make a kit worth my while.

I think there is something here for everyone.

Croup told me he’s working on more kits, maybe even some more “commercial” sounding stuff.

CROUP DON’T FREAKIN DO IT

We have plenty commercial bubble gum pop libraries for when we want to get our sexy on…please…please…please keep bringin us the funk.

How Many Subs Does Croup Get?

You know, if any kit was worth 5 subs this would be it. But I always have to push sound designers to grow…so I’ve got to go with a 4.5 out of 5 subs.

The drums knock, they can lay the proper foundation for any track…but I had to deduct a half point because he threw in some lil sexy claps.

Not that I don’t like sexy claps, but not in a collection called deadly drums or filthy drums. I don’t like to box people in, but Croup is known for those gutter, hardcore, dirty, nasty, dust in ya fingers from they backroom record collection type drums…and that’s where I want to see him live.

Many companies claim to have bangin sounds, they claim to have that punch, that meat, that dirt we need. In my years, I’ve found that few really deliver.

Croup does, plain and simple.

Go on over and checkout Croupbeatz.com and listen to the samples.

Grab the kit.

Make Bangers.

Repeat.