Author
Lars Grimm, MD, MHS
House Staff
Department of Internal Medicine
Duke University Medical Center
Durham, North Carolina
Disclosure: Lars Grimm, MD, MHS, has disclosed no relevant financial relationships.
Editor
Michael Stuart Bronze, MD
Professor, Stewart G. Wolf Chair in Internal Medicine
Department of Medicine
University of Oklahoma Health Science Center
Oklahoma City, Oklahoma
Disclosure: Michael Stuart Bronze, MD, has disclosed no relevant financial relationships.
On January 12, 2010, a major earthquake struck near Port-au-Prince, Haiti, affecting an estimated 3 million people. Given the poor infrastructure, limited healthcare facilities, and high prevalence of tropical and neglected diseases at baseline in Haiti, the potential for widespread infectious complications after the earthquake is enormous. Overcrowding, poor sanitation, and limited access to clean food and water place large numbers of individuals at risk for diarrheal, mosquito-borne, and wound infections. Governmental and nongovernmental humanitarian organizations have been actively fund raising and sending supplies and aid workers to help combat what some healthcare experts predict might be a perfect storm of medical necessity. Image courtesy of Wikimedia Commons.
The United States Geological Survey (USGS) reported a magnitude 7.0 earthquake on January 12, 2010, at 21:53:10 UTC.[1] The epicenter was located 25 km west southwest of Port-au-Prince, Haiti, at a depth of 3.4 km. The earthquake occurred along the Enriquillo-Plantain Garden fault system between the North American and Caribbean tectonic plates, the likely source of the large historical earthquakes in 1860, 1770, 1761, 1751, 1684, and 1618. The shallow depth and long duration between quakes most likely contributed to the strong intensity of the quake. Image courtesy of the US Geological Survey.
The potential infectious complications surrounding the Haitian earthquake can be broken down into several broad categories. Wound infections are a major problem, as wounds are frequently contaminated with debris, and many individuals who are trapped may go days before proper wound care can be addressed. Data collected from prior major natural disasters demonstrate that wound infections are a major source of morbidity. The destruction of infrastructure creates a dearth of clean water for drinking, bathing, and wound care. Contamination of water with sewage and fecal matter can lead to outbreaks of diarrheal illnesses. The destruction of infrastructure and breakdowns in maintenance operations can lead to pools of standing water that allow breeding of mosquitoes. Acute spikes in the incidence of mosquito-borne illnesses may be apparent. Long-term community-based strategies for preventable and chronic illnesses can be disrupted as resources and attention are redirected to more acute needs. This can lead to years of setbacks in eradication efforts.
Data collected from the 2004 tsunami in Thailand revealed that wound infections were the second most common healthcare problem among survivors.[2] Wounds were typically contaminated with debris, sand, mud, sea water, and sewage. Infections occurred usually within 72 hours. The distribution of bacterial wound cultures is shown. An increased percentage of wounds were infected with gram-negative organisms commonly found in human and animal feces. The authors recommend that a specific wound care team be created to standardize treatment for wound care.
Data collected from the 2008 earthquake in Sichuan, China, shows a different spectrum of wound cultures than in Thailand, as shown.[3] The main difference was a dramatic increase in the prevalence of Staphylococcus aureus infections, and a decrease in gram-negative infections. The authors theorize that the difference in microbial prevalence was because fewer wounds were contaminated with water in China, thus the pattern of pathogens is dependent on the environmental circumstances at the time of injury.
Cholera is a toxin-mediated diarrheal illness caused by any number of different strains of Vibrio cholerae (electron microscope image shown). Diffuse watery diarrhea induced by the cholera toxin is the hallmark of the disease. Transmission is via fecal-oral routes. The cholera toxin inhibits absorptive sodium transport and activates excretory chloride transport in the crypt cells of the small intestine. The resulting high osmolality is offset by increased luminal water secretion leading to large-volume diarrhea. Other common signs and symptoms include vomiting, hypoglycemia, hypokalemia, lethargy, tachycardia, and tachypnea. Without adequate fluid and electrolyte replacement, dehydration-induced shock and acidosis will develop. Diagnosis is typically clinical, but can be confirmed by direct microscopic examination, stool culture, or serotype testing. Oral rehydration with safe water or oral rehydration salts is typically sufficient for most patients. Empiric antibiotics, typically tetracycline, doxycycline, or ciprofloxacin, have been shown to reduce the volume of diarrhea and duration of shedding. Mortality rates for adequately treated patients are around 1%, but without access to clean water or proper sanitation, rates of 25%-50% have been reported.
Shigella organisms are gram-negative, facultative intracellular pathogens (shown) responsible for the diarrheal illness bacterial dysentery or shigellosis. Transmission is via fecal-oral routes and is a major problem in developing countries with poor sanitation. The infectivity dose is extremely low, with as few as 10 bacilli needed to cause clinical disease in some strains. Shigella spp invade the intestinal wall (shown) and release enterotoxins. The host response to primary infection is acute inflammation that leads to massive destruction of the colonic mucosa. The clinical presentation is variable and may involve cramping abdominal pain, high-grade fever, emesis, anorexia, tenesmus, fecal incontinence, watery or frankly bloody diarrhea, headache, lethargy, delirium, convulsions, hypoglycemia, dehydration, disseminated intravascular coagulation, hemolytic-uremic syndrome, and intestinal perforation. Hemolytic-uremic syndrome is microangiopathic hemolytic anemia, thrombocytopenia, and renal failure. Formal diagnosis is made by stool examination for leukocytes and blood, stool cultures, or enzyme immunoassays. Treatment involves aggressive fluid and electrolyte replacement, antipyretics, and empiric antibiotics with ampicillin or trimethoprim-sulfamethoxazole (depending on local resistance patterns). Antidiarrheal medications should be avoided because of the risk for prolonged illness. If treated, fevers typically last for 24 hours and diarrhea for 2-3 days. Mortality in the developed world is less than 1%, but it is as high as 25%-50% in the developing world. Image courtesy of the Centers for Disease Control and Prevention.
Salmonella enterocolitis is a diarrheal illness typically caused by Salmonella typhimurium (shown), Salmonella enteritidis, or Salmonella heidelberg. Transmission is typically from contaminated food, most commonly beef, poultry, and eggs. After ingestion, the Salmonella attach and then invade the cells lining the intestinal lumen, where they cause a massive efflux of fluid and electrolytes of unclear mechanism. The clinical presentation is typically large-volume watery diarrhea, fevers, abdominal cramping, chills, headache, tenesmus, and myalgias. Diarrhea typically lasts for 3-7 days. Formal diagnosis is made by stool culture. The disease is typically self-limited, and treatment involves fluid and electrolyte replacement. Antibiotics do not shorten the duration of symptoms, but may prolong the duration of convalescent carriage and are thus reserved for patients at risk for invasive disease. The mortality of uncomplicated Salmonella enterocolitis is less than 1%, but if bacteremia develops then mortality may increase to 20%-30%. Image courtesy of the National Institutes of Health.
Typhoid fever, or enteric fever, is a potentially fatal multisystemic illness caused primarily by Salmonella typhi. It is most commonly found in conditions with poor sanitation and remains endemic in developing countries. Transmission occurs via oral-fecal routes. The manifestations are protean but the classic presentation involves stepwise worsening fevers, abdominal pain, constipation, dry cough, dull frontal headaches, delirium, stuporous malaise, truncal rose spots (shown), and relative bradycardia. In the late stages, anorexia, green-yellow diarrhea, tachypnea, apathy, confusion, psychosis, myocarditis, and intestinal hemorrhage may develop. The disease course typically lasts for several weeks if untreated and can result in months of weight loss and debilitating weakness. Diagnosis is primarily clinical, but blood cultures, polymerase chain reactions, and serologic tests may be used with varying reported sensitivities and specificities. Treatment should begin before confirmation testing with antibiotic therapy, preferably fluoroquinolones or cephalosporins, depending on local resistance patterns. Corticosteroids are controversial, but may decrease the likelihood of mortality in severe cases that are complicated by neurologic changes. Mortality is 10%-20% for untreated patients and less than 1% for treated patients. Image courtesy of the Centers for Disease Control and Prevention.
Dengue fever is an acute febrile illness caused by Flavivirus spp. It is transmitted from the bite of the Aedes mosquito (pictured), which breed rapidly in stagnant water. Inoculation is immediate after a bite by an infected mosquito. During the 4- to 7-day incubation period, viral replication occurs in the dendritic cells. This is then followed by 5-7 days of febrile illness. In some patients, dengue hemorrhagic fever develops, which is the rapid onset of plasma leakage, altered hemostasis, and liver damage. Capillary fragility and thrombocytopenia lead to bleeding that ranges from petechial skin hemorrhages to life-threatening gastrointestinal bleeding. Treatment is typically supportive and acetaminophen may be used for fevers, but aspirin, nonsteroidal anti-inflammatory drugs, and corticosteroids should be avoided. Fluid and blood product resuscitation may be required for dengue hemorrhagic fever. Recovery in most patients is complete, but in hemorrhagic fever, mortality rates range from 12%-44%. There is some limited data that in prior dengue fever epidemics in Haiti there was a decreased incidence of the hemorrhagic variety, possibly suggesting a genetic or acquired advantage. Image courtesy of the Centers for Disease Control.
Malaria is a febrile, potentially life-threatening disease caused by infection with the Plasmodium protozoa. Plasmodium falciparum is the most severe of the different forms of malaria and also the most common form found in Haiti. Malaria is transmitted from the bite of an infected female Anopheles mosquito. The life cycle of the Plasmodium spp is complex and involves both liver and erythrocyte phases. Infected red blood cells rupture, releasing more parasites, a process that logarithmically increases parasite burden. The chronicity of red cell rupture is responsible for the periodicity of fevers experienced by infected individuals. In addition to fevers, patients may experience headaches, malaise, fatigue, muscle aches, and diarrhea. Severe P falciparum infection may cause cerebral malaria (coma and seizures) and anemia. Diagnosis is made with serial thick and thin blood smears. The image shown is a thin-film Giemsa stained micrograph that shows ring forms and gametocytes of P falciparum. Treatment is with chloroquine if sensitive, but because of widespread resistance, quinine sulfate plus doxycyline or clindamycin or pyrimethamine-sulfadoxine is recommended. P falciparum is responsible for 90% of the 1-3 million deaths yearly from malarial infections, most commonly from cerebral malaria. Image courtesy of the Centers for Disease Control.
Lymphatic filariasis, or elephantiasis, is a disease that causes thickening of the skin and underlying tissues from a nematodal infection. It is the second leading cause of permanent and long-term disability according to the World Health Organization. The 3 nematodes responsible for lymphatic filariasis are Wuchereria bancrofti, Brugia malayi, and Brugia timori. W bancrofti is the only species found in Latin America. Bites from infected mosquitoes deposit infective larvae into the skin. The larvae travel into the lymphatic vessels, where they grow into adult worms. Obstruction and inflammation of the lymphatic drainage causes progressive swelling and fibrosis of the affected areas (shown). In the acute phase, febrile painful lymphadenopathy may develop. Treatment with albendazole and ivermectin or diethylcarbamazine is effective. Some doctors worry that disruptions in community-based healthcare initiatives aimed at treating preventable diseases like lymphatic filariasis in Haiti will have serious long-term repercussions. Image courtesy of Wikimedia Commons.
Author
Lars Grimm, MD, MHS
House Staff
Department of Internal Medicine
Duke University Medical Center
Durham, North Carolina
Disclosure: Lars Grimm, MD, MHS, has disclosed no relevant financial relationships.
Editor
Michael Stuart Bronze, MD
Professor, Stewart G. Wolf Chair in Internal Medicine
Department of Medicine
University of Oklahoma Health Science Center
Oklahoma City, Oklahoma
Disclosure: Michael Stuart Bronze, MD, has disclosed no relevant financial relationships.
