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29 Clonorchiasis vnι.3o Croup

The Chinese liver fluke is a small worm that parasitizes the bile ducts and livers of humans, dogs, cats, pigs, and several wild animals in China, Japan, Korea, and Indochina. It was discovered in 1875, and recently, it was estimated that 20 million individuals in China alone are infected.

Eggs are laid in the bile ducts, pass in the feces, and if they reach the proper freshwater snail, undergo a series of stages in this intermediate host. Eventually, free-swimming lar­vae are formed, which penetrate and encyst the skin or muscles of fish, expecially those of the carp family. Human beings and other definitive hosts become in­fected by eating the cysts (metacercaria) in raw or poorly cooked fish. Raw fish are a delicacy in many Asian countries, and fish are sometimes raised in ponds fertilized with human feces. Encysted metacer­caria larvae are resistant to smoking, pickling, salt­ing, and drying. Imported fish have caused human cases in Hawaii, and the popularity of Asian cuisine poses a potential danger to gourmets far beyond Asia.

Light infections are often asymptomatic. Heavy infections may produce diarrhea, fever, jaundice, and abdominal pain. Bile duct blockage and liver abscesses occur in chronic cases, and Clonorchis sinensis has been tentatively linked to liver cancer. Diagnosis is made by microscopic examination of the feces to discover the characteristic eggs. Drug ther­apy is sometimes successful. Preventive measures include rural sanitation, regulation of fish-farming methods, and cooking fish thoroughly. It is unlikely, however, that long-established culinary practices can be changed.

K. David Patterson

Bibliography

Hou, P. C. 1965. The relationship between primary carci­noma of the liver and infestation with Clonorchis sinensis. Journal of Pathological Bacteriology 72: 239-46.

Kean, B. H., Kenneth E. Mott, and Adair J.

Russell, eds. 1978. Tropical medicine and parasitology: Classic in­vestigations, Vol. II, 546-60. Ithaca and London.

Kim, D. C., and R. E. Kuntz. 1964. Epidemiology of hel­minth diseases: Clonorchis sinensis (Cobbold, 1875; Looss, 1907 on Taiwan, Formosa). Chinese Medical Journal 11: 29—47.

Komiya, Y. 1966. Clonorchis and clonorchiasis. In Ad­vances in parasitology, ed. B. Dawes, 53—106. New York.

The term croup is used in an inclusive way to iden­tify several different respiratory illnesses of children manifested by varying degrees of inspiratory stridor, cough, and hoarseness due to upper-airway obstruc­tion. Classically croup was a manifestation of diph­theria. In the twentieth century, many other infec­tious causes of croup syndromes are recognized, and in addition, similar illnesses can be caused by non- infectious processes.

A classification of crouplike illnesses is presented in Table VIII.30.1. Although long-term obstruction in the glottic and subglottic regions can lead to chronic illnesses, croup syndromes are described here as acute self-limited or fatal illnesses. Most cases of croup today are either laryngotracheitis or spasmodic croup.

Etiology

Acute epiglottitis (inflammation of the epiglottis) is virtually always caused by Haemophilus influenzae type B; rare cases have been due to Streptococcus pneumoniae and Staphylococcus aureus. Laryngitis is usually due to the common respiratory viral agents, the most important of which are adeno­viruses and influenza viruses.

Laryngotracheitis and spasmodic croup are com­mon illnesses in children and are due to viruses or Mycoplasma pneumoniae. The most important agent is parainfluenza virus type 1. This virus, as well as parainfluenza type 2 and influenza A and B viruses, results in outbreaks of disease. In areas of the world

Table VIII.30.1. Classification of crouplike illnesses

Infectious Epiglottitis Laryngitis Laryngotracheitis and spasmodic croup Laryngotracheobronchitis Laryngotracheobronchiopneumonitis

Mechanical

Foreign body

Postintubation trauma

Allergic

Acute angioneurotic edema where diphtheria toxoid immunization is not carried out, laryngotracheitis is also caused by Coryne- bacterium diphtheria.

Laryngotracheobronchitis and Iaryngotracheo- bronchiopneumonitis are frequently caused by the same viruses that cause laryngotracheitis. These two illnesses are caused also by S. aureus, Streptococcus pyogenes, S. pneumoniae, and H. influenzae.

Epidemiology

Croup syndromes occur worldwide. Most illnesses are due to the common croup viruses: parainfluenza types 1 and 2 and influenza viruses. Outbreaks occur every year during the cold-weather months; in the tropics croup is more common during the rainy sea­son. The highest attack rate occurs in children 7 to 36 months of age; few cases occur in children after the sixth birthday. During the second year of life, about 5 percent of children experience an episode of croup. Croup is more common in boys than in girls and also tends to be more severe in boys.

The viruses that cause croup are present in the nasal secretions of adults and children with colds and other upper and lower respiratory tract ill­nesses. Virus is transmitted from infected persons by sneezing, nose blowing, and the general contami­nation of external surfaces (including the hands) with nasal secretions. A susceptible child can be­come infected either by inhaling virus in droplet nuclei (small particles) or by a direct nasal hit of virus-containing large droplets from a sneeze or nose blowing. Infection can also occur indirectly as a re­sult of contamination of the fingers of the recipient. It is important to emphasize that parainfluenza vi­rus infections in adults are manifested by colds; older persons with relatively trivial illnesses may be the source of severe croup in young children.

Clinical Manifestations

Acute Epiglottitis

Acute epiglottitis is a disease of relatively abrupt onset and rapid progression which, if untreated, re­sults in death due to airway obstruction. Illness is characterized by fever, severe sore throat, dys­phasia, and drooling. Airway obstruction is rapidly progressive and is associated with inspiratory dis­tress, a choking sensation, irritability, restlessness, and anxiety.

In contrast to viral croup, the patient is not hoarse and does not have the typical “croupy cough,” but the speech is muffled or thick-sounding. The child with epiglottitis insists on sitting up and will become worse and exhibit great anxiety if forced to lie down.

Patients with epiglottitis will have leukocytosis with neutrophilia and positive blood cultures for H. influenzae type B. The epiglottis is swollen and cherry red. Therapy depends upon rapid diagnosis, the establishment of an airway, and the administra­tion of antibiotics appropriate for the treatment of H. influenzae type B.

Acute Laryngotracheitis

In this section, only viral causes of croup are dis­cussed. Initial symptoms in laryngotracheitis are usually not alarming and include nasal dryness, irri­tation, and coryza (profuse nasal discharge). Cough, sore throat, and fever occur. After 12 to 48 hours, signs and symptoms of upper-airway obstruction de­velop. The cough becomes “croupy” (sounding like a sea lion), and there is increasing respiratory stridor (difficulty associated with inspiration). The degree of airway obstruction is variable. Most severe dis­ease is manifested by marked respiratory distress with supra- and infraclavicular and sternal retrac­tions, cyanosis, and apprehension. Hypoxia can oc­cur, and if there is no intervention, asphyxial death will occur in some children.

In laryngotracheitis the walls of the trachea just below the vocal cords are red and swollen. As the disease progresses, the tracheal lumen will contain fibrinous exudate, and its surface will be covered by pseudomembranes made up of exudative material. Because the subglottic trachea is surrounded by a firm cartilaginous ring, the inflammatory swelling results in encroachment on the size of the airway; it is often reduced to a slit 1 to 2 millimeters in diameter.

The treatment of laryngotracheitis includes the following: oxygen for hypoxia, fluids (locally via aero­sol and systemically) to liquefy secretions, racemic epinephrine by aerosol to decrease inflammatory edema, and rarely the establishment of the mechani­cal airway.

Corticosteroids are also frequently ad­ministered to decrease inflammation, but their use is controversial.

Spasmodic Croup

This croup is a distinct clinical syndrome, which in some instances is difficult to distinguish from mild laryngotracheitis. In contrast to laryngotracheitis in which the obstruction is due to inflammatory exu­date and cellular damage, the obstruction in spas­modic croup is due to noninflammatory edema. Ill­ness always has its onset at night, and it occurs in children thought to be well or to have a mild cold with coryza. The child awakens from sleep with sud­den dyspnea, croupy cough, and inspiratory stridor. There is no fever.

Spasmodic croup tends to run in families, and af­fected children often have repeated attacks. Treat­ment relies upon the administration of moist air and reassurance by the parents.

Acute Laryngotracheobronchitis and Laryngotracheobronchiopneumonitis

These illnesses are less common than laryngo­tracheitis and spasmodic croup but are more serious. Initial symptoms and signs are similar to those of laryngotracheitis. Usually the signs of lower respira­tory involvement develop 2 to 7 days into the illness; occasionally both upper- and lower-airway obstruc­tions occur simultaneously. In addition to the usual findings in croup, patients with Iaryngotracheo- bronchiopneumonitis will have rales, air trapping, wheezing, and an increased respiratory rate.

The illness is due to a more generalized infection with parainfluenza or influenza viruses or to secon­dary bacterial infection of the trachea, bronchi, and lungs. Exudate, pseudomembrane, and respiratory epithelial damage occur. Care involves appropriate antibiotics in addition to conventional treatment for laryngotracheitis.

History

The word croup is derived from the Anglo-Saxon word kropαn, meaning “to cry aloud.” Croup was first used in medical writing in 1765 by Francis Home, a Scot­tish physician. Until this century virtually all croup­like illnesses were confused with diphtheria.

Daniel Slade in 1864 traced the clinical history of diphtheria to the time of Homer, and A. Sanne in 1887 believed that the writings OfHippocrates dem­onstrate knowledge of diphtheria. Aretaeus of Cap­padocia, in the second century A.D., noted extension of the disease to the lower respiratory tract, which resulted in death by suffocation. Galen noted the expectoration of the pseudomembrane. At this time, the disease was common in Syria and Egypt and was called ulcus Syriacum or Egyptiacum by Aretaeus. Aetius of Amidu, in the fifth century, added his expe­riences to the previous descriptions of Aretaeus. Al­though both Aretaeus and Aetius were describing diphtheritic croup, it is clear that there was confu­sion with other illnesses such as Ludwig’s angina and streptococcal tonsillitis.

The historical trail of diphtheria disappeared in the fifth century and did not reappear until the six­teenth century: First, in 1557, Peter Forest described an epidemic in Alkuaer, Holland. Then in 1576, Guil­laume de Baillou described an epidemic in Paris and specifically commented on false membrane. In 1771 Samuel Bard published the first U.S. report on the nature, causes, and treatment of suffocative angina. Pierre Bretonneau named diphtheria in 1826 and rec­ognized its infectious nature. T. A. Edwin Klebs in 1883 noted the diphtheria bacillus in smears from pseudomembranes, and a year later Friedrich Loffler established the organism as the etiologic agent.

From 1920 to 1940 the incidence of diphtheria in the United States fell from approximately 200 cases to 20 cases per 100,000 population as a result of the use, first, of toxin-antitoxin and then of toxoid. In association with this decline in diphtheria, and also predating it, there was a general realization of other cases of croup in this century. Prior to 1900, only occasional notations of illnesses suggesting nondiph- theritic croup appeared. For example, E. Bouchut in 1852 described false croup, Stridalous laryngitis, which seems to have been spasmodic croup. In his treatise (1887), Sanne referred to an epidemic of simple croup in Germany, and Home (1765) noted two forms of croup. Bretonneau differentiated diph­theria from spasmodic croup in 1826.

In the United States during the first half of the twentieth century, severe croup was called laryngo­tracheal-bronchitis. It was recognized that it was caused by C. diphtheria bacteria and by other bacte­ria as well. In 1948, Edward Rabe described three types of croup infections: diphtheritic croup, H. influ­enzae type B croup (epiglottitis), and “virus” croup. Shortly thereafter, with the widespread use of tissue culture techniques, the viral etiology of croup was confirmed. During a period of approximately 30 years (1950-79), croup due to bacteria other than C. diph­theria was overlooked in medical papers and text­books. In 1976, nondiphtheria/bacterial croup was rediscovered, and since then it has received consider­able attention in the literature.

The history of spasmodic croup is not clear because the clinical and pathological aspects of the entity are poorly defined. In the 1940s spasmodic croup was separated from other more severe forms of croup by Francis Davison; however, since then the patho­genesis of this entity has received little attention.

James D. Cherry

Bibliography

Bouchut, E. 1859. Bouchut on croup. In Memoirs on diph­theria, ed. Robert Hunter Semple, 271—97. London.

Cherry, James D. 1981. Acute epiglottitis, Iaryngptis, and croup. In Current clinical topics in infectious diseases, ed. J. S. Remington and M. N. Swartz, 1-29. New York.

1987. Croup (laryngitis, laryngotracheitis, spasmodic croup, and Iaryngotracheobronchitis). In Textbook of pediatric infectious diseases, Vol. ∏, ed. R. D. Feigin and J. D. Cherry, 237-50. Philadelphia.

Cramblett, Henry G. 1960. Croup - present day concept. Pediatrics 25:1071-6.

Davison, Francis W. 1950. Acute obstructive laryngitis in children. Pennsylvania Medical Journal 53: 250—4.

Gittins, T. R. 1932. Laryngitis and tracheobronchitis in children: Special reference to non-diphtheritic infec­tions. Annals of Otology, Rhinology and Larynology 41: 422-38.

Guersant. 1959. Guersant on croup. In Memoirs on diph­theria, ed. Robert Hunter Semple, 207-32. London.

Home, Francis. 1765. An inquiry into the nature, cause and cure of the croup. Edinburgh.

Jacobi, A. 1880. A treatise on diphtheria. New York.

Mortimer, Edward A. 1988. Diphtheria toxoid. In Vac­cines, ed. S. A. Plotkin and E. A. Mortimer, 31-44. Philadelphia.

Nelson, Waldo E. 1950. Acute spasmodic laryngitis. In Textbook of pediatrics, ed. Waldo E. Nelson, 951. Philadelphia.

1959. Acute Iaryngotracheobronchitis. In Textbook of pediatrics, ed. Waldo E. Nelson, 778—80. Philadelphia.

1984. Bacterial croup: A historical perspective. Journal OfPediatrics 105: 52-5.

Rabe, Edward F. 1948a. Infectious croup: I. Etiology. Pedi­atrics 2: 255-65.

1948b. Infectious croup: II. “Virus” croup. Pediatrics 2: 415-27.

Sanne, A. 1887. A treatise on diphtheria. St. Louis.

Slade, Daniel D. 1864. Diphtheria: Its nature and treat­ment. Philadelphia.

Top, Franklin H. 1964. Diphtheria. In Communicable and infectious diseases, ed. F. H. Top, 217—35. Saint Louis.

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Source: Kiple Kenneth F. (Editor). The Cambridge World History of Human Disease. Cambridge University Press,1993. — 1200 p.. 1993

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