Accessed Aug 15, Urticaria and angioedema. In: Stone J, editor. Dermatologic immunology and allergy. Louis: Mosby; Demain JG. Papular urticaria and things that bite in the night. Curr Allergy Asthma Rep ; In: Demis DJ,editor. Unit Histopathologic correla- tion of lesions of papular urticaria and positive skin test reac- tions to insect antigens. Arch Dermatol Syphilol ; Walzer A, Grolnick M. The relation of papular urticaria and pru- rigo mitis to allergy.
J Allergy ; Rook A. Rook A, Frain-Bell W. Arch Dis Child ; Goldman L. Lichen urticatus syndrome as a manifestation of sensitivity to bites from various species of arthropods. Arch Dermatol Syphilol ; Papular urticaria: its relationship to insect allergy. Ann Allergy ; JAllergyClinImmunol ; Flea infestation as a cause of papular urti- caria: a preliminary investigation.
Br Med J ; Lunsford CJ. Flea problem in California. Flea infestation and its control. Int J Dermatol ; Papular urticaria: its response to treatment with DDT and the role of insect bites in its etiol- ogy. J Invest Dermatol ; Insect bites. JAMA ; Delayed reaction to bed bug bites. Arch Dermatol ; Phil- adelphia: Lippincott; Mellanby K. Nature ; Benaim-Pinto C, Fassrainer A. Int J Derma- tol ; Insect bite lesions in Kuwait possibly due to Leptodemus minutus. Histopathological studies oncutaneousreactionstothebitesofvariousarthropods.
AmJ Trop Med Hyg ; Rockwell EM, Johnson P. The insect bite reaction. J Invest Der- matol ; Gordon RM. Reactions produced by arthropods directly injuri- ous to the skin of man. Katzenellenbogen I. Acrodermatitis urticarioides. Arch Derma- tol Syphilol ; Parkhurst HJ. Trombidiosis infestation with chiggers. Ackerman AB, Bennin B. Philadelphia: Lippincott; Caputo R, Gelmetti C. Pediatric dermatology and dermatopa- thology: a concise atlas.
London: Martin Dunitz; Papular urticaria: a histopathologi- cal study of 30 patients. Am J Dermatopathol ; Delusions of parasitosis associated with coronary bypass surgery. Br J Dermatol ; Delusions of parasitosis. Ariz Med ; Lichenurticatus papularurticaria : treatment with parathyroid extract; theoretical consideration of the etiology. Am J Dis Child ; Carpet beetle dermatitis. Millikan LE. Semin Dermatol ; Localized pruritic rash due to recurrent spider bites.
J Geriatr Dermatol ; A guide to spiders and their kin. New York: Golden; Horsfall WR. Diseases caused by arthropods. In: Horsfall WR, editor. Medical entomology, arthropods and human Disease. New York: Ronald; Insectbitereactions:an update. Dermatology Basel ; Do brown recluse spider bites induce pyoderma gangrenosum? South Med J ; Brown recluse spider bites. Accessed: Aug 18, Necrotic arachnidism. Wasserman GS. Wound care of spider and snake envenoma- tion.
Ann Emerg Med ; Probable cause of necrotic spider bite in the Midwest. Science ; Nance WE. Hemolytic anemia in necrotic arachnidism. Am J Med ; Recluse spider bites: a review of reactions and treatments. Chronica Dermatol Roma ;6: Hemolytic anemia following a presump- tive brown recluse spider bite. J Toxicol Clin Toxicol ; Dissemi- nated intravascular coagulopathy following fatal brown re- cluse spider bite necrotic arachnidism. J Pediatr ; Brown recluse spi- der bites: a comparison of early surgical excision vs dapsone and delayed surgical excision.
Ann Surg ; Treatment of brown recluse spider bites. Svendsen FJ. Treatment of clinically diagnosed brown recluse spider bites with hyperbaric oxygen: a clinical observation. J Arkansas Med Soc ; Osborn DC. Treatment of spider bites by high voltage direct current. J Okla State Med Assoc ; King LE Jr. Spider bites. Horen WP. Arachnidism in the United States. JAMA ; Histopathologic analysis of hu- man bites by the brown recluse spider.
Arch Dermatol ; Berger RS. The unremarkable brown recluse spider bite. Necrotic arachnid- ism. Persistent painful plaque due to a brown recluse spider bite. Spiders and spider bites. Dermatol Clin ; Differentiating loxoscelism from Lyme disease. Emerg Med ; Lyme disease masquerading as brown recluse spider bite. Chemical burn misdiagnosed as brown re- cluse spider bite. Am J Emerg Med ; Cutaneous anthrax infection. N Engl J Med ; A new assay for the de- tection of Loxosceles species brown recluse spider venom. Antivenom treat- ment in arachnidism. J Toxicol Clin Toxicol ; Centers for Disease Control.
Loxoscelism and necrotic arach- nidism. Vest DK. Protracted reactions following probable hobo spider Tegenaria agrestis envenomation [abstract]. Am Arachnol ; Exline H. New and little known species of Tegenaria Araneida, Agelenidae. Psyche ; Gertsch WJ, Ennik F. Bull Am Museum Natural History ; Suspected Tege- naria agrestis envenomation. Ann Pharmacother ; Black widow spider bites. Latrodectism: black widow spider bites. Elston DM. Latrodectus mactans.
Clinical pre- sentationandtreatmentofblackwidowspiderenvenomation: a review of cases. Stahnke HL. Arizona Med ; Minton SA. Venom diseases. Lucas SM, Meier J. Biology and distribution of scorpions of medical importance. In: Meier J, White J, editors. Handbook of clinical toxicology of animal venoms and poisons. New York: CRC; Toxicon ; Scorpion sting in children: a review of 51 cases. Clin Pediatr ; J Toxi- col Clin Toxicol ; Warrel DA. Venomous bites and stings in the tropical world. Med J Australia ; Enveno- mation by the scorpion Centruroides sculpturatus. Envenomation by the scorpion Centru- roides exilicauda C.
Pediatrics ; Bond GR. Hemiplegia following scorpion sting. J Indian Med Assoc ; Scorpion enveno- mation. Elston DM, Stockwell S. Centruroides exili- cauda. Cutis ; , Amitai Y. Clinical manifestations and management of scorpion envenomation. Pub Health Rev ; Incidence of immediate and delayed hypersensitivity to Centruroides an- tivenom. Blankenship ML. Mite dermatitis other than scabies. Condition: New. Never used!. Seller Inventory P More information about this seller Contact this seller. Brand New!. Seller Inventory VIB Book Description Crc Press. Condition: new. Seller Inventory think Ships with Tracking Number!
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Physician’s Guide to Arthropods of Medical Importance, 5th Edition
Where breeding conditions are favorable, Culex mosquitoes also occur in enormous numbers. Several Culex species are noto- rious for their aggravating high-pitched hum when flying about the ears. In tropical areas, mosquito breeding may continue year round, but in temperate climates, many species undergo a diapause in which the adults enter a dormant state similar to hibernation. In preparation for this, females become reluctant to feed, cease ovarian development, and develop fat body.
In addition, they may seek a protected place to pass the approaching winter. Some species, instead of passing the winter as hibernating adults, produce dormant eggs or larvae that can survive the harsh effects of winter. Mosquitoes vary in their biting patterns. Most species are nocturnal in activ- ity, biting mainly in the early evening. However, some species, especially Ae. Others, such as salt marsh species and many members of the genus Psorophora do not ordinarily bite during the day, but will attack if disturbed such as walking through high grass harboring resting adults.
More people have probably died from malaria than from any other infectious disease in human his- tory.
Published estimates of the annual number of clinical cases range from to million, with several million deaths — mainly in children 3. Although many coun- tries are not entirely malarious, the WHO estimates that about 2. The geographic distribution of malaria has shrunk over the last yr, mainly from eradication efforts in temperate zones Figs.
Although indigenous malaria disappeared from the US in the s, there have been several episodes of introduced malaria and subsequent autoch- thonous cases in this country over the last two decades. Introduced malaria occurs when local people are infected as a result of imported cases travelers, and so forth or people having relapses from former cases.
Overall, the malaria situation is likely worse worldwide, because mosquito vectors are becoming resistant to many of the pesticides being used to control them, and in many areas the malaria parasites are resistant to the prophylactic drugs used to prevent the disease. There may be a repeating cycle of high fever and sweating. Infants may display only lethargy, irritability, and anorexia. In rare forms of falci- parum malaria e.
Falciparum malaria may also produce complications, such as renal failure, hemolytic anemia, hypoglycemia, and acute pulmonary edema. Diagnosis of malaria is frequently based on clinical presentation. Both thick and thin smears need to be carefully examined by lab or para- sitology personnel.
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It must be noted that a patient can be very sick and yet dem- onstrate very few parasites in blood smears. Repeated thick blood smears may be necessary every 2—6 h before the parasites are found. These immunochro- matographic tests are based on the capture of parasite antigens from peripheral blood. Recently, the U. This RDT is approved for use by hospitals and com- mercial laboratories, but not by individual clinicians or the patients themselves. The infective sporozoites are transmitted to humans only by mosquitoes in the genus Anopheles. However, not every species of Anopheles is a vector; less than half of the more than known species are considered vectors.
In fact, only 45—50 species are important vectors. Not all species of Plasmodium occur in all places. Generally, P. Navy, ref. Only a brief summary will be presented here. Sporozoties injected during mosquito biting infect liver cells. After a time of growth, development, and division, merozoites are released from the liver into the bloodstream. There the parasites invade human red blood cells, where they grow and multiply asexually. After 48—72 h, the red blood cells burst, releasing large numbers of new parasites, most of which enter new red blood cells this reinitiates the cycle.
Other than these asexual forms, some of the parasites develop into sexual forms — male and female gametocytes. If a susceptible feeding Anopheles mosquito draws up gametocytes with its blood meal, fertilization takes place in the stomach. The resulting zygote penetrates the mosquito gut wall and forms an oocyst on the basement membrane of the gut.
Eventually, oocysts rupture, releasing sporozoites inside the mosquito body cavity. After migration to the salivary glands, the mosquito is infective. The entire developmental time within the mosquito is 8—35 d. This involves several things, including the mosquito feeding on the right host, feeding in such a way or time that the parasites, circulating in the blood of the host animal, are ingested, and a mechanism for penetrating the gut wall of the mosquito and subsequently migrating to the salivary glands for reinjec- tion into another host.
All of this becomes a fine-tuned system that operates effi- ciently for countless generations. A highly efficient mosquito vector of malaria is one that is highly susceptible to the full development of the parasite Plasmodium , prefers to feed on humans, and lives for a relatively long time 3.
Some notable malaria vectors worldwide are as follows: Several members of the Anopheles gambiae complex consisting of seven almost identical species are the most efficient malaria transmitters in Africa Figs. They often breed in freshwater exposed to sunlight. Anopheles darlingi is one of the major contribu- tors to endemic malaria in extreme southern Mexico and Central and South America Figs. It breeds in shaded areas of fresh-water marshes, swamps, lagoons, lakes, and ponds.
The Anopheles leucosphyrus group containing at least 20 closely related species contains several main vectors of malaria in southeast Asia Figs. They mostly breed in freshwater pools in and among rocks, in hoofprints, vehicle ruts, and the like. It is believed that there are at least four malaria vectors in the United States — Anopheles freeborni West , An. All four of the main vector species breed in per- manent freshwater sites, such as ponds, pools, and rice fields, and are avid human biters.
Accordingly, there is always the possibility of reintroduction of the malaria parasite into the United States and resumption of indigenously acquired cases. Proper diagnosis and prompt treatment of human cases using artemisin-based combination therapies ACT see below. Wide-scale distribution and use of insecticide-treated bed nets 3. Indoor residual spraying with insecticides to reduce vector populations. There is even considerable interest currently in using DDT as an indoor residual spray 8.
Certainly, protective clothing, insect repellents, and nets for camping Fig. Bed nets impregnated with insecticide are even more effective. Since Anopheles mosquitoes mostly bite at night, use of bed netting properly employed alone can significantly reduce risk of infection.
Local vector control activities can also reduce malaria case numbers. This includes ultra-low- volume insecticide fogging, usually by truck-mounted machines, to kill adult mosquitoes outdoors, larvaciding to kill immature mosquitoes, and elimination of mosquito breeding habitats. Unfortunately, in countries with the worst malaria problems, financial resources are often unavailable for mosquito control. There are obviously several points in the complex malaria life cycle where Fig. Although many experimental vaccines have been developed and stud- ied, no practical vaccine has yet been produced.
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However, there is still hope that an effective vaccine will be developed since progress has been substantial over the past several years. At least thirty-five candidate malaria vaccines are in develop- ment, many of which are in clinical trials 9. Development of a malaria vaccine has been stymied by several factors. For one thing, the persons at greatest risk of complications and death are young children, and most researchers expect that the initial immune responses elicited by a vaccine will be suboptimal.
Second, even if a vaccine produces a vigorous humoral and cellular response, it does not necessar- ily provide sterile immunity. Even in naturally acquired infections, antibodies directed against the dominant antigen on the sporozoite surface do not prevent reinfection with sporozoites bearing the same dominant repetitive antigen. Third, for traditional vaccines, there is an inadequate number of adjuvants available for human use. For example, aluminum hydroxide is about the only adjuvant approved for human use. If other antigen—adjuvant combinations can be identified, which provide boosting with the re-exposures that occur repetitively with natural reinfec- tion under field conditions, then there is long-term promise for malaria control through vaccines.
Antimalarial drugs include chlo- roquine, amodiaquine, pyrimethamine, sulfonamides, quinine, quinidine, tetracy- clines, mefloquine, and artemisinin usually in combination with other antimalarials. Because of increased parasite resistance to antimalarial drugs, treatment regimes have become quite complicated and vary tremendously by geographic region.
In addition to the problem of resistance, serious side effects may occur with the use of some antimalarial products. Health care providers should contact their local or state health department, the CDC, or the preventive medicine department at a local medi- cal school for the most up-to-date malaria treatment recommendations.
In the United States, the most common ones are encephalitis viruses Table 3. Humans may become involved when conditions favor increased virus activity or geographic coverage. These outbreaks may be cyclical. Louis encephalitis. There was outbreak in the New Jersey — Pennsylvania region in , and another much larger outbreak in the Mississippi River Valley area in the mids 2.
Certainly not all cases of encephalitis are mosquito-caused enteroviruses and other agents are often involved , but mosquito-borne encephalitis has the potential to become a serious cause of morbidity and mortality covering widespread geographic areas of the United States each year. Although some cases may be asymptomatic, most are characterized by acute onset of headache, high fever, meningeal signs, stupor, disorientation, coma, spasticity, tremors, and convulsions 2, The disease is especially severe in children. I helped investigate a fatal case in an yr-old boy who exhibited headache, anorexia, and excessive sleepiness on the day of hospital admission.
At day three, respirations became irregular, and he eventually showed no signs of brainstem function Its appearance is seasonal; in the southernmost areas of the virus range, human cases may occur year-round, but are concentrated between May and August. EEE virus is sustained in freshwater swamps in a cycle involving birds and mosquitoes with the main enzootic vector being Culiseta melanura, which rarely bites humans or horses Fig. Epidemics in horses and humans occur when prevalence of the virus in bird populations becomes high and other mosquito species become involved.
These secondary or epizootic Fig. Other species may be involved Any cases of encephalitis in mid- to late summer should be suspect. Specific identifi- cation is usually made by finding specific IgM antibody in acute serum or cere- brospinal fluid CSF , or antibody rises usually HI test between early and late serum samples. Preventing transmission involves personal protective measures against mosquito biting, such as avoiding outdoor activity after dark, wearing long sleeves, and judicious use of repellents such as those containing the active ingredients DEET many popular brand names contain this ingredient , or picaridin, or oil of lemon eucalyptus Fig.
Caution should be exercised in applying repellents with high DEET concentrations to infants and children owing to absorption through the skin. Interrupting the EEE virus cycle in nature involves spraying the area by ground equipment or by airplane for adult mosquito control, as well as environmental sanitation efforts in affected communities to eliminate mosquito breeding sites. For example, in the fatal case of EEE men- tioned above 11 , the patient lived in a house without window screens. This likely led to increased exposure to mosquitoes and thus biting — a risk factor for any mosquito-borne disease.
This was of interest, since we take for granted the fact that basic sanitation and public health measures, such as screen wire windows, are implemented. In addition, Cq. Accordingly, control efforts were directed toward that particular mosquito species, thus averting new cases. Louis Encephalitis SLE 3. For example, in , there were 1, cases of SLE with more than deaths About 40 yr later, another major outbreak occurred in the Mississippi Valley region with over 2, cases There is usually abrupt onset of fever, headache, and malaise.
Physical exam may only reveal elevated temperature and perhaps dehydration. Over a period of several days to a week, other signs of central nervous system CNS infection may develop, such as stiff neck, disorientation, tremulousness, unsteadiness, confusion, and even coma. One elderly patient I interviewed spoke of an extreme fatigue, forcing him to bed, persisting for weeks after the infection.
The clinical features of SLE are not specific, so the illness must be differentiated from other etiologies, such as bacterial, other viral, mycobacterial, fungal, rickettsial, toxic, cerebrovascular, and neoplastic diseases Time of year may be a clue to recognizing SLE, since most cases occur in mid- to late summer. Clinical labora- tory results are generally not distinctive.
CSF may show a preponderance of poly- morphonuclear cells if obtained early in the illness; a shift toward lymphocytic pleocytosis is the rule Protein in the CSF may be slightly elevated above nor- mal during the first and second weeks of illness. Susceptible birds become viremic, and infect new mosquitoes feeding on them, which then, in turn, Fig. This cycle continues year to year, with no apparent effect on the birds or mosquitoes.
For various reasons — climatic factors or numbers of mos- quitoes or birds — the virus level in nature is amplified to the point where aberrant hosts humans become infected. Interestingly, times of drought may actually enhance SLE transmission by concentrating vector mosquitoes and bird hosts In arid regions, it is frequently found in canals and irrigation ditches. The Cx. Louis encephalitis in the western United States provided with permission by Infections in Medicine ; 3.
Many health care workers fail to realize the specificity of viruses and their hosts and vector mosquitoes. All of these fac- tors animal hosts, vector mosquitoes, and so forth are different for the particu- lar virus involved. Rarely do generalized recommendations or control schemes work. For example, once I was investigating an EEE case in an adult male patient who lived in a rural community. The health department field investigator accompanying me proceeded to tell the local people about cleaning up around their homes — removing cans, tires, and so on — where container-breeding spe- cies could live.
Since the primary inland vector of EEE in the area was a species that lived in marshes containing emergent vegetation like cattails , this health department worker was spreading misinformation and, more importantly, was not in any way helping to prevent new cases. Just as is the case with microbes in which specific control depends on the species and behavior of the organism, so it is with mosquitoes.
Control measures must be targeted toward the specific vector species involved. This outbreak of mosquito-borne encephalitis was origi- nally identified as St. Louis encephalitis SLE because the two viruses are closely related and cross reactions occur with some serological lab tests. Over the next 5 years, WNV spread across the continental U. WNV has been associated with significant human morbidity and mortality in the U. Interestingly, of the first five patients in New York City admitted to hospitals, four had severe muscle weakness and respiratory difficulty, a finding atypical for encephalitis Also, GI com- plaints such as nausea, vomiting, or diarrhea occurred in 4 of 5 patients Much remains to be learned about the ecology of WNV in the United States, but we do know the virus causes a bird disease, and is transmitted by mosquitoes.
House sparrows and robins have been found to be among the best amplifying hosts in nature, producing highest viremias for the longest period of time. Although the mosquito vector humans incidental infection animals incidental infection West Nile virus birds virus reservoir Fig. In addition, ULV adulticiding for mosquitoes with truck-mounted or airplane-mounted sprayers can be useful in reducing popula- tions of vector mosquitoes. Personal protection measures include long sleeves and long pants when outdoors, proper screening and netting, and use of insect repellents.
There were large epidemics in the north central United States in and in the central valley of California in 2. The outbreak involved 3, cases. There was a large outbreak a few years ago in West Virginia. Serological and epidemiological stud- ies in North Carolina, Georgia, Tennessee, Mississippi, Virginia, and Florida have indicated that LAC occurs and is increasing in those states also, but not to the extent that it currently occurs in the midwestern United States.
Interestingly, LAC virus may be transferred from adult female Oc. Some amplification of the virus takes place in nature through an Oc. The virus is transmitted by many mosquito species, particularly those in the genus Psorophora. The mosquito, Oc. In an outbreak in Venezuela in —, there were more than 23, reported human cases with deaths 2. A more recent outbreak in Colombia and Venezuela resulted in at least 75, human cases JE is highly virulent. The virus is transmitted by several Culex mosquitoes, but especially Cx.
JE epidemics have, at times, been widespread and quite severe. Historically, JE has been focused in the northern areas of countries in southeast Asia, east Asia, and midsouthern Asia, especially China and Vietnam Fig. Recently, there has been a steady westward extension of reported epi- demic activity into northern India, Nepal, and Sri Lanka. JE has the potential for introduction and establishment in North America, especially via international travel and smuggling of animals and legal exotic pets The geographic distribution of CHIK has historically included most of Sub-Saharan Africa, India, Southeast Asia, Indonesia, and the Philippines, although the disease is increasing both in incidence and geographic range.
There were , cases on Reunion Island in the Indican Ocean during — India suffered an explo- sive outbreak in with more than 1. The virus, a flavivirus related to yellow fever virus, has four sero- types Den 1, Den 2, Den 3, and Den 4 and is transmitted to people primarily by the mosquitoes, Ae. As far as is known, humans are the main vertebrate reservoir of the virus, although there may be a monkey-mosquito cycle in some areas.
Hundreds of cases occurred in the summer of along the Texas—Mexico border, especially in the Reynosa area. A few cases were acquired on the US side. There is always the possibility of a widespread dengue epidemic in the United States since there is an abundance of the mosquito vectors in the south central United States.
Also, with the thousands of people returning home from cruises to the Caribbean each month especially during the summer , there is good chance of infected persons returning and infecting local mosquitoes with the virus. Mosquitoes may become infected by feeding on viremic patients, generally only from the day before to the end of the febrile period Usually, they will not feed again for 3—5 d, depending on temperature. It is in this second or third, rarely feeding when a susceptible person is inoculated with the virus.
The adult lifespan of dengue vec- tor mosquitoes is generally very short few days , although some may survive 14 d or longer. Accordingly, it is amazing that dengue virus transmission occurs at all. However, mosquito populations are so great, that even though most females die before feeding a second time, enough individuals survive long enough to keep virus transmission going. Prime sites include paint cans, old tires, urns and jars, clogged rain gutters, pet watering dishes, etc.
Aedes albopictus, known as the Asian tiger mosquito, was accidentally introduced into the United States from Japan in in the Houston, Texas area. Since then, it has rapidly spread over much of the central and southern United States, often replacing the native Ae. Today, the Asian tiger mosquito is the primary pest mosquito in many towns and cities, being extremely difficult to control by standard mosquito spraying trucks or airplane because of its close proximity to houses and daytime feeding habit. After an incubation period of 5—8 d, there is sudden onset of fever, severe headache, retro-orbital pain, myalgia, and arthralgia.
There may also be GI disturbances, mottling of the skin, and rash. This list comes from Halstead Sex: Shock cases and deaths occur more frequently in female than male children. Preceding host conditions: Menstrual periods and peptic ulcers are risk factors for the severe bleeding in adults, which occurs during some dengue infections. However, the hypovolemic shock resulting from DHF may require several specific interventions see an appropri- ate clinical text for current guidelines.
Both of these require public educa- tion campaigns. Since the traditional ultra-low-volume insecticide sprays are mostly ineffective against these species, elimination of larval breeding sources is needed. This requires convincing the public and property owners of the need for such activity. Special clean-up days may need to be proclaimed by government officials to promote elimination of breeding sites around homes remember, this species is not ordinarily found deep in the woods or swamps. If necessary, spe- cial teams of health department or volunteer evaluators may be formed to walk through every neighborhood, inspecting premises, dumping out water-filled con- tainers, and possibly treating other breeding sites with pesticide.
However, development of an effective vaccine for dengue is fraught with difficulty. In other words, the severe hemorrhagic manifestations are believed to occur as a result of sequential infec- tion by more than one dengue virus serotype. Apparently, infection-enhancing antibodies are raised to antigens shared between the first and second infecting serotypes. Therefore, much thought must be given to the problem of the possibil- ity of immune potentiation in dengue infection in any vaccine development study.
The avoidance of ADE is one reason why, in the development of whole virus vaccines, it is necessary to produce a tetravalent formulation 41 , but the use of tetravalent formulations of attenuated viruses may run into problems of emer- gence of revertants to virulent forms or to domination of one or another serotype owing to the well-known phenomenon of viral interference Some of these problems are being addressed by using infectious cDNA clones to design chi- meric constructs containing genes of one dengue virus in a background of another. Therefore, it may be possible to create a DNA vaccine for dengue It consists of a sylvatic form — that can occa- sionally spread to humans — circulating among forest monkeys in Africa and Central and South America, and an urban form transmitted by the peridomestic mosquito, Aedes aegypti, without any involvement of monkeys 5, 43 Fig.
Jaundice is usually moderate early in the disease and intensified later After the initial clinical syndrome, there may be a brief remission lasting from several hours to a day. Published sensational accounts often mention profuse vomiting of black material, collapse, and sudden death. YF is caused by a flavivirus that is transmitted to humans by the bite of infected mosquitoes.
Even though an effective vaccine is available, there is still a significant disease burden in Africa and South America from YF. Although it can occur from Mexico to Argentina, most cases in the Americas occur in northern South America and the Amazon Basin, including the Colombian llanos extensive plains and eastern regions of Peru and Boliva.
Interestingly, YF does not occur in India or the densely populated coun- tries of southeast Asia, even though plentiful vector mosquitoes and monkeys occur there. Historically, YF epidemics have hit European seaports and many American towns and cities with devastating results see Sect. YF must never be ignored lest it be reintroduced into nonendemic areas via fast-paced air travel. The vector mosquitoes are ever present; all that is needed is the introduc- tion of the etiologic agent.
In fact, there was an imported case of YF in a yr- old man who returned to Tennessee from a 9-d trip to Brazil Reportedly, he had visited the jungles of Brazil along the Rio Negro and Amazon Rivers and had not been previously vaccinated. The man died 6 d after hospital admission and 10 d after his first symptoms appeared. New Orleans, Memphis, and Philadelphia were among the hardest hit In , one of every ten Philadelphians died.
In New Orleans during a major outbreak in , there were 29, cases with over 8, deaths. One of the worst American epi- demics occurred in involving towns, 75, cases, and 16, deaths. During that epidemic, Memphis was devastated 48, Panic ensued. People with financial resources fled, leaving behind only the poor, sick, or dying. The city was considered dead.
Ramsey of Washington, who came to Memphis with a corps of Howard Association nurses 49 : Memphis is a city of horrors. The poor whites and Negroes from miles around Memphis have flocked into the city looking for food. Hundreds of them prowl around the streets with hardly any clothes on…. They break into the vacant houses whenever they want.
The stench of Memphis sickened me before I got within 5 miles of the city. No words can describe the filth I saw, the rotten wooden pavements, the dead animals, putrefying human bodies, and the half-buried dead combining to make the atmosphere something fearful. I took 30 grains of quinine and drops of tincture of iron every day and wore a thick veil soaked with carbolic acid over my face. Many of the nurses, both men and women, smoke cigars constantly while attending patients to ward off the stench.
In the Peabody Hotel where I stayed, pans of sulphur were kept burning in the halls. Eventually, scientific research began to shed light on the etiology of YF and its link to mosquitoes. In , Carlos Finlay, a Cuban physician, was the first to suggest that the disease was transmitted by a mosquito 50 , but little was done to evaluate the claim until the establishment of a US Army Commission Board in Cuba in which set out to systematically investigate YF.
The United States had won control of Cuba at the end of the Spanish-American War in , and accordingly, many US military personnel were stationed there. Attempts to prove a bacterial etiology for YF were negative. In fact, the causative agent of YF was shown to pass through bacteriological filters, indicating a viral etiology.
This was the first demonstration of a human disease caused by a virus James Carroll, Dr.
Aristides Agramonte, and Jessee W. Lazear — designed several amazing experiments to unravel the YF mystery systematically. In subsequent tests, the volunteers had to sleep on pillows covered with towels soaked with blood of YF victims All volunteers remained well. The fomite theory of YF transmission was now history. Mosquitoes that had previously been fed on sick patients were released into one side of the house where a susceptible host — John Moran — reclined, clothed in only a nightshirt.
He was bitten repeatedly. Other susceptible volunteers were asked to sleep in the other side of the house free from mosquitoes. Five days later Moran came down with classic YF, but the others remained healthy. The Board then made a far-reaching conclusion: regardless of its cause, YF must be transmitted by mosquitoes, and therefore can be managed by mosquito control and patient isolation techniques.
Interestingly, many of the brave volunteers the ones who got sick or stayed in the fomite house who participated in these YF experiments were eventually awarded a Congressional Medal of Honor. Public health officials must dili- gently monitor jungle YF activity as it may be bridged into urban areas. In , the largest jungle YF epidemic in history recorded cases with deaths In Africa, key links in the jungle cycle are Cercopithecidae monkeys includes red-tailed monkeys , and more rarely, the lesser bush-baby, infected by tree can- opy mosquitoes, such as Aedes africanus Other mosquito species may be involved, especially in bridging the sylvatic cycle to an urban cycle.
The virus can be introduced to urban areas in several ways. Villagers may acquire the virus while working in the forest and then return home ill, or infected red-tailed mon- keys may venture into villages looking for food and be bitten by peridomestic mosquitoes. In the Americas, the sylvatic hosts are in the family Cebidae — espe- cially howler and spider monkeys.
Vector mosquitoes maintaining the sylvatic cycle include many species of Haemagogus mosquitoes. These mosquitoes breed in tree holes within dense forests, but will bite humans if given the opportunity — situations like woodcutters clearing forests for agriculture. The urban cycle begins as these sickened foresters go back to their villages. The urban cycle human-to- human in both Africa and the Americas is maintained by domestic Ae. This vaccine is one of the most success- ful live attenuated vaccines known to science. It is highly immunogenic, has a very low incidence of clinical reactions, and confers long-lasting possibly lifetime immunity.
The package insert should be consulted before vaccine administration for advice about specific restrictions or exclusions e. Transmission of YF may also be interrupted by mosquito avoidance, control, and, specifically, destruction of Ae. Understanding the dynamics of urban YF gives one a unique perspective of the historical aspects of the disease. Discovering the urban mosquito vector — the exploitable weak link — was the key to stopping epidemics. At first, no one knew what spread the disease; it was just known that it moved in waves from one place to another.
Some physicians logically assumed that fomites articles of bedding or clothing contaminated with the agent must be the cause. Others believed that YF was spread by miasmatic poisoned air. Fear and panic ruled during epidemics. People were often held at bay at gunpoint, prevented from entering towns. No one knew at the time that the real problem was mosquito breeding!
It seems odd that something as simple as a clean-up campaign, combined with mosquito avoidance screens or nets , could so drastically reduce human suffering and death owing to this terrible disease. Only species affecting the lymphatic system are discussed here. Other species that may occasionally infect human tissues are included in the next section. There are at least million people at risk of lym- phatic filariasis in 76 countries, and some 79 million people actually infected There are basically two types of this mosquito-borne disease, relating to the species of round worm involved — Bancroftian filariasis and Brugian sometimes also called Malayan filariasis.
A third type, Timoran filariasis, is rare and limited to a very small geographic area, and will not be addressed in this chapter. Filariasis occurs over much of the tropical world, whereas the Brugian form is mostly confined to southeast Asia 12 Figs. Clinical symptoms include fever, lymphangitis, lymphadenitis, occasional abscess formation, and chronic obstructive manifestations.
The obstructive sign, elephantiasis, is thought by many to be the inevitable end result of filariasis; however, elephantiasis is actually an uncommon complication. Millions of immigrants have come to the United States in the last decade, many originating from countries with endemic filariasis. Others develop inflammatory manifestations, such as an acute localized inflammation the skin may be erythematous and hot , lymphadenitis, lymphangi- tis, and fever. There may be accompanying chills, sweats, headache, anorexia, lethargy, myalgias, and arthralgias.
Abscesses may arise in the inguinal and axillary lymphatic structures, distal extremities, or breasts. Inflammation of the testicles, epididymus, and spermatic cord may also result. Obstructive filaria- sis may occur when adult worms in the inguinal or other lymph nodes cause obstruction of lymphatic drainage resulting in the legs or scrotum swelling to gro- tesque proportions. As this condition continues, it becomes stabilized and hardened by fibrosis — a condition called elephantiasis. Elephantiasis generally only develops in a small number of people who have been exposed to filarial infections repeatedly over a period of years.
Hypereosinophilia is a common laboratory finding. Microfilariae may be directly viewed microscopi- cally Fig. Each of the tiny worms is inside a thin, delicate sheath — the persisting egg mem- brane Fig. Presence or absence of the sheath is important. Other species of nonpathogenic filariae may infect humans, which produce unsheathed microfilar- iae, but all pathogenic ones are sheathed. It must be noted that filarial infection may occur without detectable microfilaremia.
There was at one time a small endemic center of the disease near Charleston, SC that has apparently disappeared Bancroftian filariasis is an interesting disease in that there are no other known vertebrate hosts of the worms. It is transmitted solely by mosquitoes, and there is no multiplication of the parasite in the mosquito vector.
The house mosquito, Culex quinquefasciatus, is a common urban vector; in rural areas, transmission is maintained mainly by Anopheles mosquitoes 43, The disease has been virtually eradicated from Sri Lanka and Taiwan, and nearly so from main- land China. The life cycle of the causative agent, Brugia malayi, is similar to that of W. However, Anopheles mosquitoes may also be involved.
Some forms of Brugian filariasis may involve animal reservoirs, such as cats, monkeys, and pangolins. They penetrate the mosquito stomach wall, entering the body cavity hemo- coel , where they migrate to flight muscles for growth. After two molts, the third- stage infective larvae migrate through the head, eventually reaching the proboscis of the mosquito.
By this time, the larvae are 1. In humans, the parasites pass to the lymphatic system where they undergo further molts eventually to become adult worms several months later. Adult worms may live in humans — almost con- tinuously producing thousands of microfilariae per day — for 10—18 yr 12, Much has been written about periodicity; it has classically been said that the pro- portion of number of microfilariae found in blood smears during the day as opposed to night is Nonetheless, Bancroftian filariasis generally displays periodicity over much of its range a subperiodic form does occur, however , whereas Malayan filariasis has several forms — nocturnal periodic, nocturnal subperiodic, and possibly a diur- nal subperiodic from DEC is an extremely effective micro- filaricide for Wuchereria and Brugia species, resulting in near-zero micro- filaremia levels within hours, and one or more treatment courses may kill most of the adult worms DEC is contraindicated in pregnant women and persons with renal disease.
There may be systemic aller- gic reactions associated with rapid clearance of the microfilariae, but they usually can be managed with antipyretics, antihistamines, and analgesics. Over the last decade, the veterinary drug, ivermectin Mectizan , has shown great promise in treatment of various filarial diseases, such as onchocerciasis. This drug has the advantage over DEC in its efficacy when given as a single dose. Ivermectin for use in lymphatic filariasis is considered investigational at this time 54, Examples include the causative agents of Bancroftian and Malayan filariasis discussed above , loiasis, onchocerciasis, and dirofilariasis dog heartworm.
Other filarial worms may or may not cause symptomatic disease and are less well known and thus have no common name , such as Mansonella ozzardi, Mansonella streptocerca, Mansonella perstans, Dirofilaria tenuis, Dirofilaria ursi, Dirofilaria repens, and others. The dog heartworm, Dirofilaria immitis, occurs mainly in the tropics and sub- tropics, but also extends into southern Europe and North America. This worm infects several canid species, sometimes cats, and, rarely, humans.
Numerous mos- quito species are capable of transmitting dog heartworm, especially those in the genera Aedes, Anopheles, Ochlerotatus, and Culex. Mosquitoes pick up the micro- filariae with their blood meal when feeding on infected dogs. In endemic areas, a fairly high infection rate may occur in local mosquitoes. Undoubtedly, thousands of people in the United States are bitten each year by mosquitoes infected with D.
Physician’s Guide to Arthropods of Medical Importance, 5th Edition
Fortunately, humans are accidental hosts, and the larvae usually die. However, they may occasionally be found as a subadult worm in the lung seen as a coin lesion on X-ray exam The incidence of dog heartworm in humans may well be decreasing in the United States because of wide- spread — and fairly consistent — treatment of domestic dogs for heartworm. The closely related D.
See if you can figure out which encephalitis virus was involved in each case. I assure you, they are common ones. While your diagnostic decisions will be hampered by lack of specific laboratory findings, other clues — such as age of the patient, relative severity of the illness, clinical presentation, and kinds of mosquitoes collected — are revealed in the case histories. Case 1. In late June , a six-month-old, previously healthy infant was brought to an emergency department ED with a several-hour history of fever, with a maximum temperature of He was experienc- ing a focal seizure characterized by uncontrollable blinking of the left eye, twitching of the left side of the mouth, and random tongue movement.