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Tropical hygiene. Hygienic description of climate and weather of hot and low latitudes (features of sun radiation, vibrations of days and seasonal parameters of microclimate). Features of influencing of tropical climate are on the terms of life, capacity and health of population. Hygienic toxicological and epidemiology problems in feeding of population of tropical regions. 1
THE PLAN • Introduction • Hygienically characteristic of the climate • The heating microclimate and its influence on the human organism • Diarrhea in the returning traveler. • Poisonous plants and fish. • Mushroom poisoning.
Koeppen climate classification The Köppen system recognizes five major climate types based on the annual and monthly averages of temperature and precipitation. Each type is designated by a capital letter. A - Moist Tropical Climates are known for their high temperatures year round and for their large amount of year round rain. B - Dry Climates are characterized by little rain and a huge daily temperature range. Two subgroups, S - semiarid or steppe, and W - arid or desert, are used with the B climates. C - In Humid Middle Latitude Climates land/water differences play a large part. These climates have warm, dry summers and cool, wet winters. D - Continental Climates can be found in the interior regions of large land masses. Total precipitation is not very high and seasonal temperatures vary widely. E - Cold Climates describe this climate type perfectly. These climates are part of areas where permanent ice and tundra are always
Processes of Thermal Transfer Thermoregulation of human organism on 85 % is realized through the skin. The most way of the heat losses oforganism by radiation is 45 %, by convection and conduction 30 %, by evaporation (perspiration)10 % . .
Hyperthermia Hyperthermia in its advanced state referred to as heat stroke or sunstroke, is an acute condition which occurs when the body produces or absorbs more heat than it can dissipate. It is usually due to excessive exposure to heat. The heat-regulating mechanisms of the body eventually become overwhelmed and unable to effectively deal with the heat, and body temperatureclimbs uncontrollably
Traveler's diarrhea affects some 30 to 50% of visitors to developing countries. • In general, travelers at risk for diarrhea commonly come from industrialized nations and travel to high-risk areas that are primarily within developing or less industrialized nations of the world, including Latin America, Africa, the Middle East and Asia. Areas of lesser risk include China and some Caribbean nations.
What causes traveler's diarrhea?Travelers' diarrhea usually is contracted by the ingestion of contaminated food or water. Contrary to common belief, food, not water, is primarily at fault. Most cases of travelers' diarrhea are caused by bacteria. The single most important bacterium is enterotoxigenic E. coli which has been estimated to account for up to 70% of all cases.
Also the CAUSES OF traveler's diarrhea ARE: • Campylobacter jejuni • Shigella • Salmonella • Viruses (including Rotavirus, Norwalk virus and other enteric viruses) less commonly are causes of travelers' diarrhea. • The parasites Giardia lamblia, Cryptosporidium, Strongyloides stercoralis , and Entamoeba histolytica may cause prolonged illnesses characterized by weight loss (with Giardia or Cryptosporidium), vague abdominal symptoms, perianal itching, occasional wheezing and eosinophilia (with Strongyloides), or rarely, invasive amebic colitis.
CLINICAL SYMPTOMS of Diarrhea • Diarrhea in travelers is usually between 5 and 15 days after arrival. • Main symptoms: • malaise, • anorexia, • nausea, • occasional vomiting, • watery diarrhea that may be explosive and profuse. • Fever, if present, is usually low grade. • The majority of traveler's diarrhea is noninflammatory, without blood or pus in the stools. Illnesses are usually self-limited, lasting 2 to 5 days, but some may extend beyond 10 to 14 days. Patients with prolonged diarrhea after travel to developing areas present special problems.
It is important to consider and recognize potentially serious systemic infections such as malaria and, typhoid fever that may be acquired in tropical areas and present with diarrhea. These life-threatening infections usually present with higher fevers and must be evaluated by blood smears and cultures and treated promptly when suspected. Other considerations may include plague, typhus, melioidosis, and arboviral hemorrhagic fevers
DIAGNOSIS The diarrhea usually is mild, self-limited, and resolves spontaneously. Although new gene probes for enterotoxins are becoming increasingly available, most immunologic, tissue culture, and animal assays for ETEC remain research tools and are not necessary in sporadic cases of traveler's diarrhea. Inflammatory processes that may warrant bacterial culture or parasite examinations includehigh fever, tenesmus, bloody dysentery, and prolonged illnesses with weight loss. If there is any suspicion of an inflammatory, bloody, or prolonged diarrheal illness, a prompt microscopic examination of fresh samples for fecal leukocytes (with methylene blue or Gram's stain) and for parasites should be done. Although one may see motile trophozoites of Giardia lamblia or Entamoeba histolytica, special stains for amebae (e.g., trichrome stain, with micrometer measurements of parasite size), Cryptosporidium and Isospora belli (with modified acid-fast stain), or Strongyloides (with Baermann's funnel gauze concentration) may be necessary .A history of recent antibiotic use, especially if inflammatory diarrhea follows, should prompt a consideration of colitis caused by C. difficile cytotoxin .The increasing frequency of acquired immunodeficiency syndrome (AIDS) should also broaden the considerations of diarrhea causes to include additional viruses (e.g., cytomegalovirus or herpesvirus) as well as parasites (especially Cryptosporidium and /. belli), bacteria (e.g., Salmonella, Campylobacter, Mycobacteria, and others) and even fungi (e.g., Candida) agents.
PREVENTION The prevention of traveler's diarrhea includes the avoidance of salads, raw vegetables, untreated or unboiled water or ice, dairy products uncooked meat or seafood which can reduce risk, even in highly endemic areas. Even bottled, non-carbonated water or beverages may not be safe, as outbreaks of cholera and typhoid fever have been traced to bottled drinks.
POISONOUS PLANTS AND FISH Toxic and poisonous plants and animals exist in all environments. The numerical richness of tropical flora and fauna increases the relative number of toxic species. Poisonings are increasing in frequency. This increase is related directly to increased exposure. Several factors are involved in this increase. Development of natural resources in the tropics has opened vast areas to immigration, which exposes a native population to new toxins and poisons. The same development, coupled with technological progress in processing and transportation of foodstuffs, permits wide dissemination of occasionally toxic foods, usually fish or shellfish. Distribution occurs often before their toxicity can be recognized. The resultant increase in population at risk is followed by an increase in numbers of poisonings.
FISH POISONING
What is fish poisoning? There are 500 species of known toxic fish; most are reef fish. At certain times of the year, various species of fish and shellfish contain poisonous biotoxins, even if well cooked. In some fish, all the tissues are toxic; in others, only the tissues of certain organs are toxic. Reef fish from the tropical and subtropical waters of the West Indies, the Pacific Ocean, and the Indian Ocean pose the greatest threat. Most common fish poisonings are: CIGUATERA POISONING TETRAODON POISONING SCOMBROID POISONING
CIGUATERA POISONING is the most important type of poisoning. Three hundred species of fish have been incriminated in a wide geographic distribution from the West Indies to the Pacific. The ciguatoxic fish cannot be recognized by external appearance. Species that are toxic in one locality may be nontoxic in another. This illness is caused by eating fish that contain toxins produced by a marine microalgae called Gambierdiscus toxicus.
Types of fish which may contain the toxin at unpredictable times includeciguatera fish, red snapper, grouper, amberjack, sea bass, and a wide range of tropical reef fish. Ciguatera fish
Clinical Manifestations and Prognosis Clinical manifestations of poisoning occurs 4 to 30 hours after ingestion. In the main, the manifestations are gastrointestinal and neurological, with nausea (and, on occasion, a metallic taste in the mouth), vomiting and diarrhea, abdominal pain and cramps, paresthesiaaround the mouth (and in some cases the fingers and toes), cold-to-hot sensory reversal dysesthesia, increased salivation, dilatation of the pupils, strabismus, ptosis, weakness, myalgia of the legs, incoordination, and even paralysis. The mortality rate is as high as 10%. Usually, death occurs from respiratory failure or hypovolemic shock.
TETRAODON POISONING Tetrodotoxin, also called pufferfish poisoning or fugu poisoning, is a much more rare form of fish poisoning, but is potentially very serious. This is almost exclusively associated with the consumption of the pufferfish from waters of the Indo-Pacific regions, but there have been several reported cases of poisonings, including fatalities, from pufferfish in the Atlantic Ocean, Gulf of Mexico, and Gulf of California. Pufferfish poisoning is a continuing problem for Japan.
Tetraodon-toxin, a neurotoxin, is widely distributed among the order Tetraodontoidea (Plectognathi). This includes puffers (blowfish, toadfish, fugu), ocean sunfish, and porcupine fish.
Those kinds of fish are characterized by having very small scales. The toxin concentrates mainly in: the liver, ovaries, intestine, and skin of the fish. Puffer musculature is generally considered nonpoisonous. Toxicity is related to the reproductive cycle, being highest just before spawning in late spring or early summer.
Symptoms generally appear between 20 minutes to 3 hours after eating the poisonous pufferfish. The most common symptoms of pufferfish poisoning are: numbness of lips, tongue, throat and late, the limbs abdominal pain dizziness headache vomiting diarrhea sweating extensive muscle weakness There is a tachycardia, hypotension, and, increasing difficulty with breathing, which may be complicated by a general flaccid ascending paralysis, leading to respiratory failure, convulsions, and death in 6 to 24 hours.
Treatment for pufferfish poisoning (TETRAODON POISONING): Treatment for pufferfish poisoning consists of limiting the body's absorption of the toxin, relieving symptoms, and treating life-threatening complications. There is no known antidote for tetrodotoxin.
SCOMBROID POISONING Scromboid poisoning occurs after eating fish that contain high levels of histamine. These fish, which include mahi mahi (dolphin fish), albacore tuna, bluefin and yellowfin tuna, mackerel, and sardines, have high amounts of histidine. As a result of inadequate refrigeration or preservation, bacteria (Proteus, Salmonella, Clostridium, and Escherichia coli)convert the histidine to histamine, and this leads to scromboid poisoning. This form of fish poisoning occurs worldwide in temperate and tropical waters.
Clinical Symptoms: Signs and symptoms occur about 3 hours after ingestion of the fish. an acute allergic or histamine-like reaction, with headache; flushing of the head and upper trunk; generalized urticaria; swelling of the eyelids, periorbital tissue, lips, tongue, and throat; muscular weakness; myalgia; diarrhea. Recovery usually takes place in about 3 to 16 hours, although occasional deaths have been reported.
OTHER FISH POISONINGS • Elasmobranch PoisoningThis occurs after ingestion of the liver or skeletal muscles of sharks and rays. The symptoms usually occurs after 30 minutes. These are usually mild following ingestion of the musculature and include some abdominal pain but mainly diarrhea. Symptoms are more severe after ingestion of the liver and include, in addition to diarrhea and abdominal pain, nausea, vomiting, headache, tingling around the mouth, and a burning sensation of the tongue. In severe cases, this may progress to ataxia, visual disturbances, difficulty with breathing, coma, and death. Most patients, however, recover completely in 5 to 20 days.
Hallucinatory Fish Poisoning • This may occur after ingestion of certain species of mullet. Signs and symptoms begin about 2 hours after ingestion of the fish and are all neurologic, e.g., incoordination, nightmares, ataxia, and hallucinations. No fatalities have been recorded, and cathartics are recommended in treatment. • Miscellaneous • Other intoxications have been described, e.g., fish roe poisoning, fish blood poisoning, and fish liver poisoning. • The contamination of the sea and its fauna by metallic wastes, particularly mercury, has been described in Japan, i.e., Minamata disease.
SHELLFISH POISONING • Clinically, there are 3 types of shellfish poisoning • GASTROINTESTINAL • ALLERGIC • PARALYTIC
GASTROINTESTINAL SHELLFISH POISONING The symptoms: nausea, vomiting, diarrhea, and abdominal pain, occur 8 to 12 hours after ingestion. Bacterial contamination of the shellfish is believed to be the cause. ALLERGIC SHELLFISH POISONING The symptoms: skin rash and itching, nasal congestion, dryness of the throat, and edema of the tongue, causing potentially fatal respiratory distress, occur 30 minutes to 6 hours after ingestion. It is thought to be due to individual sensitivity to the shellfish.
PARALYTIC SHELLFISH POISONING This is also called dinoflagellate poisoning and saxitoxin poisoning. This is an acute poisoning due to saxitoxin, a powerful curare like neurotoxin that is produced by toxic species of planktonic dinoflagellates and concentrated in filter-feeding mollusks (clams, oysters, scallops, mussels). The principal action of the toxin occurs centrally on the respiratory and vasomotor centers and peripherally at the neuro-muscular junctions and the sensory nerve endings. The symptoms are: paresthesia starts in the lips and tip of the tongue and spreads to involve the face, scalp, neck, and extremities. There may also be weakness of the limbs, ataxia, incoherent speech, aphonia, tightness of the throat and chest, and increased salivation, the pulse is thready; superficial reflexes may be lost, is usually 30 minutes after the ingestion of the shellfish. If the patient survives the first 12 hours, the prognosis is good. However, the mortality rate is 1 to 7%, with death usually occurring from respiratory paralysis within 24 hours.
Many plants have responded to the challenge for survival by evolving chemical toxins and irritants to fend off animals. That’s why many plants can cause a disease as a result of inadvertent ingestion or contact. Generally plant toxins pose the greatest hazard for young children and visitors new to an environment. Toxin concentrations vary with season, the maturity of the plant, and geographic origin. Not all parts of a plant need be toxic. In many areas methods of food preparation have been evolved to detoxify the plant material. The processing of bitter manioc, Manihot utilissima, is one example. Rapid, inexpensive transportation of fresh foodstuffs, coupled with a keen interest in culinary experimentation, has greatly enhanced the possible exposure to toxic plants. In addition to plant toxins, mycotoxins and external and internal environmental contaminants can cause disease. Pesticide residues pose the most common hazard.
Datura stramonium (Jimson-weed; moon-lily; Jamestown weed) FAMILY: Solanaceae—the Nightshade Family PHENOLOGY: Datura flowers June through August. DISTRIBUTION: Jimson-weed occurs over the world, usually as an inhabitant of dry soil and waste places, dumps, abandoned fields, and in cultivated crops, especially soybeans and corn. POISONOUS PARTS: All parts are poisonous, especially seeds and leaves. Lethal dosages for cattle may be 10-14 oz (0.06-0.09% of the animal's body weight). It is estimated that 4-5 g of leaf or seeds would be fatal to a child. SYMPTOMS:intense thirst, visual disturbance, flushed skin, and central nervous system hyperirritability. Victims become delirious, incoherent, and perform insensible antics. Heart beat may be rapid with elevated temperature. Subjects may be prone to violence, hallucination, convulsions, coma, and death.
POISONOUS PRINCIPLES: Solanaceous alkaloids (tropane configuration) including atropine, hyosayamine (isomeric with atropine), and hyoscine (scopolamine). Datura alkaloids are useful in medicine. Total content of alkaloids in a plant may be high, varying from 0.25-.0.7%. Concentration varies in different parts of the plant, during various stages of development, and under varied growing conditions. The alkaloids are fewer following a rainy period than during clear, dry weather, and concentration decreases during the day but increases at night. OF INTEREST: American Indians utilized this plant for medicinal and religious purposes. Soldiers sent in 1676 to quell the Bacon rebellion at Jamestown, Virginia experienced mass poisoning due to this plant; hence, the common name Jamestown weed. Because of the hallucinogenic properties of deadly Datura, Europeans learned to boil and incorporate plant extracts into fats or oils. These extracts were rubbed on the skin or orifice areas (rectum, vagina) to induce hallucinogenic "flights from reality". .
